TY  - CONF
AU  - Jović, Milena
AU  - Simeunović, Valentina
AU  - Vukojević, Anđela
AU  - Prvulović, Milica
AU  - Sokanović, Srđan
AU  - Mladenović, Aleksandra
AU  - Milanović, Desanka
AU  - Todorović, Smilja
AU  - Lončarević-Vasiljković, Nataša
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5851
AB  - According to the amyloid hypothesis of Alcheimer’s disease (AD), disruption of 
balance between production and clearance of Aβ from the cells leads to the 
progressive accumulation and aggregation of amyloid beta (Aβ) peptides in the brain. 
The glial system (microglial cells and astrocytes) is responsible for maintaining 
homeostasis in the brain which implies its important role in the development and 
progression of AD. Our previous work revealed that the short-term fish oil (FO) 
treatment in 5xFAD mice, (AD animal model), reduces toxic Aβ load and increases 
number of microglial/macrophage cells in parietal cortex. In the present study we 
aimed to further decipher the roles of microglial and macrophage cells and to 
elucidate possible mechanisms responsible for observed reduced level of toxic Aβ42 
peptide. For this purpose, western blot and immunohistochemical analysis were used 
to detect changes in parietal cortex of three-month-old 5xFAD mice after three weeks 
FO treatment (100μl/animal/day). Distinction between microglial cells and 
macrophages was assessed using double immunostaining with anti-TMEM119 and 
anti-Iba1 antibodies respectively. Immunostaining was observed by confocal 
microscopy. For western blot analysis anti-TREM-2 and anti-IDE were used to 
observe potential mechanism responsible for extracellular clearance of toxic Aβ 
forms. Quantification was done by Image Quant software. Our results showed that 
short-term FO supplementation affects the localization and number of microglial cells 
and macrophages. Macrophages were located around the plaque and were responsible 
for the formation of a mechanical barrier, while microglial cells showed an increased 
number under the treatment and were located far from the plaques. Furthermore, the 
treatment did not seem to affect the level of IDE, while on the other hand it 
significantly increased the level of TREM-2 (ultimately sustaining the microglial 
response to Aβ-plaque-induced pathology).
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia
T1  - Short-term fish oil treatment increases number of microglial cells  and expression level of TREM-2 in parietal cortex of 5XFAD mice
SP  - 65
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5851
ER  - 

@conference{
author = "Jović, Milena and Simeunović, Valentina and Vukojević, Anđela and Prvulović, Milica and Sokanović, Srđan and Mladenović, Aleksandra and Milanović, Desanka and Todorović, Smilja and Lončarević-Vasiljković, Nataša",
year = "2023",
abstract = "According to the amyloid hypothesis of Alcheimer’s disease (AD), disruption of 
balance between production and clearance of Aβ from the cells leads to the 
progressive accumulation and aggregation of amyloid beta (Aβ) peptides in the brain. 
The glial system (microglial cells and astrocytes) is responsible for maintaining 
homeostasis in the brain which implies its important role in the development and 
progression of AD. Our previous work revealed that the short-term fish oil (FO) 
treatment in 5xFAD mice, (AD animal model), reduces toxic Aβ load and increases 
number of microglial/macrophage cells in parietal cortex. In the present study we 
aimed to further decipher the roles of microglial and macrophage cells and to 
elucidate possible mechanisms responsible for observed reduced level of toxic Aβ42 
peptide. For this purpose, western blot and immunohistochemical analysis were used 
to detect changes in parietal cortex of three-month-old 5xFAD mice after three weeks 
FO treatment (100μl/animal/day). Distinction between microglial cells and 
macrophages was assessed using double immunostaining with anti-TMEM119 and 
anti-Iba1 antibodies respectively. Immunostaining was observed by confocal 
microscopy. For western blot analysis anti-TREM-2 and anti-IDE were used to 
observe potential mechanism responsible for extracellular clearance of toxic Aβ 
forms. Quantification was done by Image Quant software. Our results showed that 
short-term FO supplementation affects the localization and number of microglial cells 
and macrophages. Macrophages were located around the plaque and were responsible 
for the formation of a mechanical barrier, while microglial cells showed an increased 
number under the treatment and were located far from the plaques. Furthermore, the 
treatment did not seem to affect the level of IDE, while on the other hand it 
significantly increased the level of TREM-2 (ultimately sustaining the microglial 
response to Aβ-plaque-induced pathology).",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia",
title = "Short-term fish oil treatment increases number of microglial cells  and expression level of TREM-2 in parietal cortex of 5XFAD mice",
pages = "65",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5851"
}

Jović, M., Simeunović, V., Vukojević, A., Prvulović, M., Sokanović, S., Mladenović, A., Milanović, D., Todorović, S.,& Lončarević-Vasiljković, N.. (2023). Short-term fish oil treatment increases number of microglial cells  and expression level of TREM-2 in parietal cortex of 5XFAD mice. in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 65.
https://hdl.handle.net/21.15107/rcub_ibiss_5851

Jović M, Simeunović V, Vukojević A, Prvulović M, Sokanović S, Mladenović A, Milanović D, Todorović S, Lončarević-Vasiljković N. Short-term fish oil treatment increases number of microglial cells  and expression level of TREM-2 in parietal cortex of 5XFAD mice. in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia. 2023;:65.
https://hdl.handle.net/21.15107/rcub_ibiss_5851 .

Jović, Milena, Simeunović, Valentina, Vukojević, Anđela, Prvulović, Milica, Sokanović, Srđan, Mladenović, Aleksandra, Milanović, Desanka, Todorović, Smilja, Lončarević-Vasiljković, Nataša, "Short-term fish oil treatment increases number of microglial cells  and expression level of TREM-2 in parietal cortex of 5XFAD mice" in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia (2023):65,
https://hdl.handle.net/21.15107/rcub_ibiss_5851 .

TY  - JOUR
AU  - Ivković, Sanja
AU  - Major, Tamara
AU  - Mitić, Miloš
AU  - Lončarević-Vasiljković, Nataša
AU  - Jović, Milena
AU  - Adžić, Miroslav
PY  - 2022
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0024320522001709
UR  - http://www.ncbi.nlm.nih.gov/pubmed/35283177
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4942
AB  - The brain is the softest organ in the body, and any change in the mechanical properties of the tissue induces the activation of glial cells, astrocytes and microglia. Amyloid plaques, one of the main pathological features of Alzheimer's disease (AD), are substantially harder than the surrounding brain tissue and can activate astrocytes and microglia resulting in the glial engulfment of plaques. Durotaxis, a migratory preference towards stiffer tissue, is prompting microglia to form a mechanical barrier around plaques reducing amyloid β (Aβ) induced neurotoxicity. Mechanoreceptors are highly expressed in the brain, particularly in microglia. The large increase in the expression of the mechanoreceptor Piezo1 was observed in the brains from AD animal models and AD patients in plaque encompassing glia. Importantly, Piezo1 function is regulated via force-from-lipids through the lipid composition of the membrane and membranous incorporation of polyunsaturated fatty acids (PUFAs) can affect the function of Piezo1 altering mechanosensitive properties of the cell. On the other hand, PUFAs dietary supplementation can alter microglial polarization, the envelopment of amyloid plaques, and immune response and Piezo1 activity was implicated in the similar modulations of microglia behavior. Finally, PUFAs treatment is currently in use in medical trials as the therapy for sickle cell anemia, a disease linked with the mutations in Piezo1. Further studies are needed to elucidate the connection between PUFAs, Piezo1 expression, and microglia behavior in the AD brain. These findings could open new possibilities in harnessing microglia in AD and in developing novel therapeutic strategies.
T2  - Life sciences
T1  - Fatty acids as biomodulators of Piezo1 mediated glial mechanosensitivity in Alzheimer's disease.
VL  - 297
DO  - 10.1016/j.lfs.2022.120470
SP  - 120470
ER  - 

@article{
author = "Ivković, Sanja and Major, Tamara and Mitić, Miloš and Lončarević-Vasiljković, Nataša and Jović, Milena and Adžić, Miroslav",
year = "2022",
abstract = "The brain is the softest organ in the body, and any change in the mechanical properties of the tissue induces the activation of glial cells, astrocytes and microglia. Amyloid plaques, one of the main pathological features of Alzheimer's disease (AD), are substantially harder than the surrounding brain tissue and can activate astrocytes and microglia resulting in the glial engulfment of plaques. Durotaxis, a migratory preference towards stiffer tissue, is prompting microglia to form a mechanical barrier around plaques reducing amyloid β (Aβ) induced neurotoxicity. Mechanoreceptors are highly expressed in the brain, particularly in microglia. The large increase in the expression of the mechanoreceptor Piezo1 was observed in the brains from AD animal models and AD patients in plaque encompassing glia. Importantly, Piezo1 function is regulated via force-from-lipids through the lipid composition of the membrane and membranous incorporation of polyunsaturated fatty acids (PUFAs) can affect the function of Piezo1 altering mechanosensitive properties of the cell. On the other hand, PUFAs dietary supplementation can alter microglial polarization, the envelopment of amyloid plaques, and immune response and Piezo1 activity was implicated in the similar modulations of microglia behavior. Finally, PUFAs treatment is currently in use in medical trials as the therapy for sickle cell anemia, a disease linked with the mutations in Piezo1. Further studies are needed to elucidate the connection between PUFAs, Piezo1 expression, and microglia behavior in the AD brain. These findings could open new possibilities in harnessing microglia in AD and in developing novel therapeutic strategies.",
journal = "Life sciences",
title = "Fatty acids as biomodulators of Piezo1 mediated glial mechanosensitivity in Alzheimer's disease.",
volume = "297",
doi = "10.1016/j.lfs.2022.120470",
pages = "120470"
}

Ivković, S., Major, T., Mitić, M., Lončarević-Vasiljković, N., Jović, M.,& Adžić, M.. (2022). Fatty acids as biomodulators of Piezo1 mediated glial mechanosensitivity in Alzheimer's disease.. in Life sciences, 297, 120470.
https://doi.org/10.1016/j.lfs.2022.120470

Ivković S, Major T, Mitić M, Lončarević-Vasiljković N, Jović M, Adžić M. Fatty acids as biomodulators of Piezo1 mediated glial mechanosensitivity in Alzheimer's disease.. in Life sciences. 2022;297:120470.
doi:10.1016/j.lfs.2022.120470 .

Ivković, Sanja, Major, Tamara, Mitić, Miloš, Lončarević-Vasiljković, Nataša, Jović, Milena, Adžić, Miroslav, "Fatty acids as biomodulators of Piezo1 mediated glial mechanosensitivity in Alzheimer's disease." in Life sciences, 297 (2022):120470,
https://doi.org/10.1016/j.lfs.2022.120470 . .

TY  - JOUR
AU  - Mladenović, Aleksandra
AU  - Kapetanou, Marianna
AU  - Lončarević Vasiljković, Nataša
AU  - Todorović, Smilja
AU  - Athanasopoulou, Sofia
AU  - Jović, Milena
AU  - Prvulović, Milica
AU  - Taoufik, Era
AU  - Matsas, Rebecca
AU  - Kanazir, Selma
AU  - Gonos, Efstathios S.
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4074
AB  - Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by a progressive decline in a variety of cognitive and non-cognitive functions. The amyloid beta protein cascade hypothesis places the formation of amyloid beta protein aggregates on the first position in the complex pathological cascade leading to neurodegeneration, and therefore AD might be considered to be a protein-misfolding disease. The Ubiquitin Proteasome System (UPS), being the primary protein degradation mechanism with a fundamental role in the maintenance of proteostasis, has been identified as a putative therapeutic target to delay and/or to decelerate the progression of neurodegenerative disorders that are characterized by accumulated/aggregated proteins. The purpose of this study was to test if the activation of proteasome in vivo can alleviate AD pathology. Specifically by using two compounds with complementary modes of proteasome activation and documented antioxidant and redox regulating properties in the 5xFAD transgenic mice model of AD, we ameliorated a number of AD related deficits. Shortly after proteasome activation we detected significantly reduced amyloid-beta load correlated with improved motor functions, reduced anxiety and frailty level. Essentially, to our knowledge this is the first report to demonstrate a dual activation of the proteasome and its downstream effects. In conclusion, these findings open up new directions for future therapeutic potential of proteasome-mediated proteolysis enhancement.
PB  - Elsevier Inc.
T2  - Free Radical Biology and Medicine
T1  - Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation
VL  - 162
DO  - 10.1016/j.freeradbiomed.2020.11.038
SP  - 88
EP  - 103
ER  - 

@article{
author = "Mladenović, Aleksandra and Kapetanou, Marianna and Lončarević Vasiljković, Nataša and Todorović, Smilja and Athanasopoulou, Sofia and Jović, Milena and Prvulović, Milica and Taoufik, Era and Matsas, Rebecca and Kanazir, Selma and Gonos, Efstathios S.",
year = "2021",
abstract = "Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by a progressive decline in a variety of cognitive and non-cognitive functions. The amyloid beta protein cascade hypothesis places the formation of amyloid beta protein aggregates on the first position in the complex pathological cascade leading to neurodegeneration, and therefore AD might be considered to be a protein-misfolding disease. The Ubiquitin Proteasome System (UPS), being the primary protein degradation mechanism with a fundamental role in the maintenance of proteostasis, has been identified as a putative therapeutic target to delay and/or to decelerate the progression of neurodegenerative disorders that are characterized by accumulated/aggregated proteins. The purpose of this study was to test if the activation of proteasome in vivo can alleviate AD pathology. Specifically by using two compounds with complementary modes of proteasome activation and documented antioxidant and redox regulating properties in the 5xFAD transgenic mice model of AD, we ameliorated a number of AD related deficits. Shortly after proteasome activation we detected significantly reduced amyloid-beta load correlated with improved motor functions, reduced anxiety and frailty level. Essentially, to our knowledge this is the first report to demonstrate a dual activation of the proteasome and its downstream effects. In conclusion, these findings open up new directions for future therapeutic potential of proteasome-mediated proteolysis enhancement.",
publisher = "Elsevier Inc.",
journal = "Free Radical Biology and Medicine",
title = "Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation",
volume = "162",
doi = "10.1016/j.freeradbiomed.2020.11.038",
pages = "88-103"
}

Mladenović, A., Kapetanou, M., Lončarević Vasiljković, N., Todorović, S., Athanasopoulou, S., Jović, M., Prvulović, M., Taoufik, E., Matsas, R., Kanazir, S.,& Gonos, E. S.. (2021). Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation. in Free Radical Biology and Medicine
Elsevier Inc.., 162, 88-103.
https://doi.org/10.1016/j.freeradbiomed.2020.11.038

Mladenović A, Kapetanou M, Lončarević Vasiljković N, Todorović S, Athanasopoulou S, Jović M, Prvulović M, Taoufik E, Matsas R, Kanazir S, Gonos ES. Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation. in Free Radical Biology and Medicine. 2021;162:88-103.
doi:10.1016/j.freeradbiomed.2020.11.038 .

Mladenović, Aleksandra, Kapetanou, Marianna, Lončarević Vasiljković, Nataša, Todorović, Smilja, Athanasopoulou, Sofia, Jović, Milena, Prvulović, Milica, Taoufik, Era, Matsas, Rebecca, Kanazir, Selma, Gonos, Efstathios S., "Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation" in Free Radical Biology and Medicine, 162 (2021):88-103,
https://doi.org/10.1016/j.freeradbiomed.2020.11.038 . .

TY  - JOUR
AU  - Carregosa, Diogo
AU  - Mota, Sara
AU  - Ferreira, Sofia
AU  - Alves-Dias, Beatriz
AU  - Lončarević-Vasiljković, Nataša
AU  - Crespo, Carolina Lage
AU  - Menezes, Regina
AU  - Teodoro, Rita
AU  - Santos, Cláudia Nunes dos
PY  - 2021
UR  - https://www.mdpi.com/2072-6643/13/9/2940
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC8464690
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4475
AB  - The rise of neurodegenerative diseases in an aging population is an increasing problem of health, social and economic consequences. Epidemiological and intervention studies have demonstrated that diets rich in (poly)phenols can have potent health benefits on cognitive decline and neurodegenerative diseases. Meanwhile, the role of gut microbiota is ever more evident in modulating the catabolism of (poly)phenols to dozens of low molecular weight (poly)phenol metabolites that have been identified in plasma and urine. These metabolites can reach circulation in higher concentrations than parent (poly)phenols and persist for longer periods of time. However, studies addressing their potential brain effects are still lacking. In this review, we will discuss different model organisms that have been used to study how low molecular weight (poly)phenol metabolites affect neuronal related mechanisms gathering critical insight on their potential to tackle the major hallmarks of neurodegeneration.
T2  - Nutrients
T1  - Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms.
IS  - 9
VL  - 13
DO  - 10.3390/nu13092940
SP  - 2940
ER  - 

@article{
author = "Carregosa, Diogo and Mota, Sara and Ferreira, Sofia and Alves-Dias, Beatriz and Lončarević-Vasiljković, Nataša and Crespo, Carolina Lage and Menezes, Regina and Teodoro, Rita and Santos, Cláudia Nunes dos",
year = "2021",
abstract = "The rise of neurodegenerative diseases in an aging population is an increasing problem of health, social and economic consequences. Epidemiological and intervention studies have demonstrated that diets rich in (poly)phenols can have potent health benefits on cognitive decline and neurodegenerative diseases. Meanwhile, the role of gut microbiota is ever more evident in modulating the catabolism of (poly)phenols to dozens of low molecular weight (poly)phenol metabolites that have been identified in plasma and urine. These metabolites can reach circulation in higher concentrations than parent (poly)phenols and persist for longer periods of time. However, studies addressing their potential brain effects are still lacking. In this review, we will discuss different model organisms that have been used to study how low molecular weight (poly)phenol metabolites affect neuronal related mechanisms gathering critical insight on their potential to tackle the major hallmarks of neurodegeneration.",
journal = "Nutrients",
title = "Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms.",
number = "9",
volume = "13",
doi = "10.3390/nu13092940",
pages = "2940"
}

Carregosa, D., Mota, S., Ferreira, S., Alves-Dias, B., Lončarević-Vasiljković, N., Crespo, C. L., Menezes, R., Teodoro, R.,& Santos, C. N. d.. (2021). Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms.. in Nutrients, 13(9), 2940.
https://doi.org/10.3390/nu13092940

Carregosa D, Mota S, Ferreira S, Alves-Dias B, Lončarević-Vasiljković N, Crespo CL, Menezes R, Teodoro R, Santos CND. Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms.. in Nutrients. 2021;13(9):2940.
doi:10.3390/nu13092940 .

Carregosa, Diogo, Mota, Sara, Ferreira, Sofia, Alves-Dias, Beatriz, Lončarević-Vasiljković, Nataša, Crespo, Carolina Lage, Menezes, Regina, Teodoro, Rita, Santos, Cláudia Nunes dos, "Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms." in Nutrients, 13, no. 9 (2021):2940,
https://doi.org/10.3390/nu13092940 . .

TY  - JOUR
AU  - Potrebić, Milica
AU  - Pavković, Željko
AU  - Lončarević-Vasiljković, Nataša
AU  - Kanazir, Selma
AU  - Pešić, Vesna
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4073
AB  - Reduction in direct social contact with peers during early adolescence is thought to be a risk factor for an increase in depressive symptoms, but there is still no clear evidence to suggest early behavioral manifestations and their association with the later outcome of social distancing during this period. To address this question, we used social isolation paradigm in peripubertal rats as the rodent model of adolescence. The litter was an experimental unit. On postnatal day 29, each litter gave group-housed and single-housed males, which were reared and tested one week and two weeks thereafter. Psychomotor/emotional response to novelty in exploration-based tasks, behavioral and neuronal responses to the drug reward (D-amphetamine), motivation/hedonic behavior, physiological and response to physiological stress were examined. Social isolation in peripubertal rats manifested through: hyper-reactivity/agitation and the state anxiety/risk-taking at an early stage; reduced behavioral response to D-amphetamine and altered neural processing of this stimulus, at a later stage; consummatory hypohedonia that deepened over time without changing the motivation to eat; unchanged body weight gain and resting blood corticosterone, cortisol and glucose levels over time; altered blood biochemistry (silenced corticosterone and increased glucose) due to overnight fasting only at an early stage. Our results highlight that the outcome of reduced direct social contact with peers during peripuberty is dynamic, with the cluster of atypical early symptoms that evolve into the syndrome that is delicate for assessment through routinely measurable behavior and biomarkers of stress, but with progressive consummatory hypohedonia and unaffected motivation to eat as stable marks.
PB  - Elsevier Inc.
T2  - Progress in Neuro-Psychopharmacology and Biological Psychiatry
T1  - Altered hedonic, novelty-, stress- and D-amphetamine-induced response to due to social isolation in peripuberty
VL  - 108
DO  - 10.1016/j.pnpbp.2020.110186
SP  - 110186
ER  - 

@article{
author = "Potrebić, Milica and Pavković, Željko and Lončarević-Vasiljković, Nataša and Kanazir, Selma and Pešić, Vesna",
year = "2021",
abstract = "Reduction in direct social contact with peers during early adolescence is thought to be a risk factor for an increase in depressive symptoms, but there is still no clear evidence to suggest early behavioral manifestations and their association with the later outcome of social distancing during this period. To address this question, we used social isolation paradigm in peripubertal rats as the rodent model of adolescence. The litter was an experimental unit. On postnatal day 29, each litter gave group-housed and single-housed males, which were reared and tested one week and two weeks thereafter. Psychomotor/emotional response to novelty in exploration-based tasks, behavioral and neuronal responses to the drug reward (D-amphetamine), motivation/hedonic behavior, physiological and response to physiological stress were examined. Social isolation in peripubertal rats manifested through: hyper-reactivity/agitation and the state anxiety/risk-taking at an early stage; reduced behavioral response to D-amphetamine and altered neural processing of this stimulus, at a later stage; consummatory hypohedonia that deepened over time without changing the motivation to eat; unchanged body weight gain and resting blood corticosterone, cortisol and glucose levels over time; altered blood biochemistry (silenced corticosterone and increased glucose) due to overnight fasting only at an early stage. Our results highlight that the outcome of reduced direct social contact with peers during peripuberty is dynamic, with the cluster of atypical early symptoms that evolve into the syndrome that is delicate for assessment through routinely measurable behavior and biomarkers of stress, but with progressive consummatory hypohedonia and unaffected motivation to eat as stable marks.",
publisher = "Elsevier Inc.",
journal = "Progress in Neuro-Psychopharmacology and Biological Psychiatry",
title = "Altered hedonic, novelty-, stress- and D-amphetamine-induced response to due to social isolation in peripuberty",
volume = "108",
doi = "10.1016/j.pnpbp.2020.110186",
pages = "110186"
}

Potrebić, M., Pavković, Ž., Lončarević-Vasiljković, N., Kanazir, S.,& Pešić, V.. (2021). Altered hedonic, novelty-, stress- and D-amphetamine-induced response to due to social isolation in peripuberty. in Progress in Neuro-Psychopharmacology and Biological Psychiatry
Elsevier Inc.., 108, 110186.
https://doi.org/10.1016/j.pnpbp.2020.110186

Potrebić M, Pavković Ž, Lončarević-Vasiljković N, Kanazir S, Pešić V. Altered hedonic, novelty-, stress- and D-amphetamine-induced response to due to social isolation in peripuberty. in Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2021;108:110186.
doi:10.1016/j.pnpbp.2020.110186 .

Potrebić, Milica, Pavković, Željko, Lončarević-Vasiljković, Nataša, Kanazir, Selma, Pešić, Vesna, "Altered hedonic, novelty-, stress- and D-amphetamine-induced response to due to social isolation in peripuberty" in Progress in Neuro-Psychopharmacology and Biological Psychiatry, 108 (2021):110186,
https://doi.org/10.1016/j.pnpbp.2020.110186 . .

TY  - JOUR
AU  - Mladenović, Aleksandra
AU  - Lončarević Vasiljković, Nataša
AU  - Gonos, Efstathios S.
PY  - 2021
UR  - https://pubmed.ncbi.nlm.nih.gov/32242468/
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4208
AB  - Significance: It is well established that lifestyle and dietary habits have a tremendous impact on life span, the rate of aging, and the onset/progression of age-related diseases. Specifically, dietary restriction (DR) and other healthy dietary patterns are usually accompanied by physical activity and differ from Western diet that is rich in fat and sugars. Moreover, as the generation of reactive oxidative species is the major causative factor of aging, while DR could modify the level of oxidative stress, it has been proposed that DR increases both survival and longevity. Recent Advances: Despite the documented links between DR, aging, and oxidative stress, many issues remain to be addressed. For instance, the free radical theory of aging is under "re-evaluation,"while DR as a golden standard for prolonging life span and ameliorating the effects of aging is also under debate. Critical Issues: This review article pays special attention to highlight the link between DR and oxidative stress in both aging and age-related diseases. We discuss in particular DR's capability to counteract the consequences of oxidative stress and the molecular mechanisms involved in these processes. Future Directions: Although DR is undoubtedly beneficial, several considerations must be taken into account when designing the best dietary intervention. Use of intermittent fasting, daily food reduction, or DR mimetics? Future research should unravel the pros and cons of all these processes. Antioxid. Redox Signal. 34, 421-438.
PB  - Mary Ann Liebert Inc.
T2  - Antioxidants and Redox Signaling
T1  - Dietary Restriction and Oxidative Stress: Friends or Enemies?
IS  - 5
VL  - 34
DO  - 10.1089/ars.2019.7959
SP  - 421
EP  - 438
ER  - 

@article{
author = "Mladenović, Aleksandra and Lončarević Vasiljković, Nataša and Gonos, Efstathios S.",
year = "2021",
abstract = "Significance: It is well established that lifestyle and dietary habits have a tremendous impact on life span, the rate of aging, and the onset/progression of age-related diseases. Specifically, dietary restriction (DR) and other healthy dietary patterns are usually accompanied by physical activity and differ from Western diet that is rich in fat and sugars. Moreover, as the generation of reactive oxidative species is the major causative factor of aging, while DR could modify the level of oxidative stress, it has been proposed that DR increases both survival and longevity. Recent Advances: Despite the documented links between DR, aging, and oxidative stress, many issues remain to be addressed. For instance, the free radical theory of aging is under "re-evaluation,"while DR as a golden standard for prolonging life span and ameliorating the effects of aging is also under debate. Critical Issues: This review article pays special attention to highlight the link between DR and oxidative stress in both aging and age-related diseases. We discuss in particular DR's capability to counteract the consequences of oxidative stress and the molecular mechanisms involved in these processes. Future Directions: Although DR is undoubtedly beneficial, several considerations must be taken into account when designing the best dietary intervention. Use of intermittent fasting, daily food reduction, or DR mimetics? Future research should unravel the pros and cons of all these processes. Antioxid. Redox Signal. 34, 421-438.",
publisher = "Mary Ann Liebert Inc.",
journal = "Antioxidants and Redox Signaling",
title = "Dietary Restriction and Oxidative Stress: Friends or Enemies?",
number = "5",
volume = "34",
doi = "10.1089/ars.2019.7959",
pages = "421-438"
}

Mladenović, A., Lončarević Vasiljković, N.,& Gonos, E. S.. (2021). Dietary Restriction and Oxidative Stress: Friends or Enemies?. in Antioxidants and Redox Signaling
Mary Ann Liebert Inc.., 34(5), 421-438.
https://doi.org/10.1089/ars.2019.7959

Mladenović A, Lončarević Vasiljković N, Gonos ES. Dietary Restriction and Oxidative Stress: Friends or Enemies?. in Antioxidants and Redox Signaling. 2021;34(5):421-438.
doi:10.1089/ars.2019.7959 .

Mladenović, Aleksandra, Lončarević Vasiljković, Nataša, Gonos, Efstathios S., "Dietary Restriction and Oxidative Stress: Friends or Enemies?" in Antioxidants and Redox Signaling, 34, no. 5 (2021):421-438,
https://doi.org/10.1089/ars.2019.7959 . .

TY  - CONF
AU  - Prvulović, Milica
AU  - Todorović, Smilja
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Kanazir, Selma
AU  - Mladenović, Aleksandra
PY  - 2020
UR  - https://forum2020.fens.org/
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5824
AB  - Objectives: Increased frailty is associated with the progression of Alzheimer’s disease (AD), characterized by the accumulation of amyloid plaques composed of aggregated amyloid-beta (Abeta) peptides, mainly Abeta 42. It has been shown that substances like 18 alpha- glycyrrhetinic acid (18-alpha GA) are able to enhance activity of ubiquitin-proteasome system responsible for the removal of proteins, and to decrease Abeta deposits in model organisms. We examined the effect of 18-alpha GA supplementation on APP processing and generation of Abeta 42 in the 5xFAD transgenic AD mouse model, characterized by the deposition of plaques in the cortex and hippocampus as early as at 2 months of age.
Methods: Both female and male mice were exposed to the 18-alpha GA treatment for six months, starting from 2-months of age which is considered an early phase of AD pathology, suitable for therapeutics application. Frailty was determined in control young (2 months) and old (12-13 months of age) mice, as well in those treated with 18-alpha-GA, by using phenotype frailty score (FS) and clinical frailty index (FI).  
Results: Obtained results showed a significant increase in frailty in aged 5xFAD mice. Significant differences were observed between males and females. 18-alpha-GA treatment increased activity of the proteasome in the cortex and hippocampus of 5xFAD mice, decreased the number of Abeta plaques and decreased frailty level.
Conclusions: Results indicate that 18-alpha-GA has a therapeutic potential in treatment of AD pathology.
PB  - Federation of European Neuroscience Societies
C3  - 12 FENS Forum of Neuroscience; 2020 Jul 11-15; Virtual Forum
T1  - Frailty in 5xFAD mouse model of Alzheimer’s disease: The influence of age and proteasome activation
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5824
ER  - 

@conference{
author = "Prvulović, Milica and Todorović, Smilja and Jović, Milena and Lončarević-Vasiljković, Nataša and Kanazir, Selma and Mladenović, Aleksandra",
year = "2020",
abstract = "Objectives: Increased frailty is associated with the progression of Alzheimer’s disease (AD), characterized by the accumulation of amyloid plaques composed of aggregated amyloid-beta (Abeta) peptides, mainly Abeta 42. It has been shown that substances like 18 alpha- glycyrrhetinic acid (18-alpha GA) are able to enhance activity of ubiquitin-proteasome system responsible for the removal of proteins, and to decrease Abeta deposits in model organisms. We examined the effect of 18-alpha GA supplementation on APP processing and generation of Abeta 42 in the 5xFAD transgenic AD mouse model, characterized by the deposition of plaques in the cortex and hippocampus as early as at 2 months of age.
Methods: Both female and male mice were exposed to the 18-alpha GA treatment for six months, starting from 2-months of age which is considered an early phase of AD pathology, suitable for therapeutics application. Frailty was determined in control young (2 months) and old (12-13 months of age) mice, as well in those treated with 18-alpha-GA, by using phenotype frailty score (FS) and clinical frailty index (FI).  
Results: Obtained results showed a significant increase in frailty in aged 5xFAD mice. Significant differences were observed between males and females. 18-alpha-GA treatment increased activity of the proteasome in the cortex and hippocampus of 5xFAD mice, decreased the number of Abeta plaques and decreased frailty level.
Conclusions: Results indicate that 18-alpha-GA has a therapeutic potential in treatment of AD pathology.",
publisher = "Federation of European Neuroscience Societies",
journal = "12 FENS Forum of Neuroscience; 2020 Jul 11-15; Virtual Forum",
title = "Frailty in 5xFAD mouse model of Alzheimer’s disease: The influence of age and proteasome activation",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5824"
}

Prvulović, M., Todorović, S., Jović, M., Lončarević-Vasiljković, N., Kanazir, S.,& Mladenović, A.. (2020). Frailty in 5xFAD mouse model of Alzheimer’s disease: The influence of age and proteasome activation. in 12 FENS Forum of Neuroscience; 2020 Jul 11-15; Virtual Forum
Federation of European Neuroscience Societies..
https://hdl.handle.net/21.15107/rcub_ibiss_5824

Prvulović M, Todorović S, Jović M, Lončarević-Vasiljković N, Kanazir S, Mladenović A. Frailty in 5xFAD mouse model of Alzheimer’s disease: The influence of age and proteasome activation. in 12 FENS Forum of Neuroscience; 2020 Jul 11-15; Virtual Forum. 2020;.
https://hdl.handle.net/21.15107/rcub_ibiss_5824 .

Prvulović, Milica, Todorović, Smilja, Jović, Milena, Lončarević-Vasiljković, Nataša, Kanazir, Selma, Mladenović, Aleksandra, "Frailty in 5xFAD mouse model of Alzheimer’s disease: The influence of age and proteasome activation" in 12 FENS Forum of Neuroscience; 2020 Jul 11-15; Virtual Forum (2020),
https://hdl.handle.net/21.15107/rcub_ibiss_5824 .

TY  - CHAP
AU  - Smiljanić, Kosara
AU  - Lončarević-Vasiljković, Nataša
AU  - Kanazir, Selma
AU  - Mladenović, Aleksandra
PY  - 2020
UR  - http://www.eurekaselect.com/node/182407
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3965
AB  - Cholesterol is the molecule essential for life, but also with a possible detrimental role. Apart from being a vital structural constituent of the cells, cholesterol is a factor involved in many important cell processes. However, it has been known that high blood cholesterol is associated with many pathological conditions. An elevated level of cholesterol is linked with cardiovascular disease, diabetes and neurodegenerative disorders. Almost quarter of the total cholesterol in the body resides in the brain. This vast pool is synthesized in situ and it is almost completely isolated and independent from the periphery due to the presence of blood-brain barrier. In the central nervous system, cholesterol plays important role in neural cells structure and functions, including synaptic transmission. Due to this, its content must be precisely maintained in order to keep brain function well. However, cholesterol is critically challenged in the aging brain and disturbed in several of pathological conditions, like Huntington’s disease (HD), Parkinson’s disease (PD), Niemann-Pick type C (NPC) disease and Smith-Lemli Opitz syndrome (SLOS), traumatic brain injury, multiple sclerosis (MS) and in Alzheimer’s disease (AD). Altered cholesterol metabolism has been extensively implicated in the pathogenesis of AD. A growing amount of evidence underscores the link between disturbed intracellular trafficking of cholesterol in the brain and the formation of amyloid plaques. The inheritance of the epsilon4 allele of the Apolipoprotein E (ApoE), the main transport protein for cholesterol in the brain represents the main risk factor for late onset form of Alzheimer’s disease. Other genetic polymorphisms associated with critical points in cholesterol metabolism may also contribute to the AD pathogenesis. Hypercholesterolemia has been considered nowadays also as a risk factor, and all of these players are thought to promote the production of beta-amyloid and development of AD. Additional proof towards cholesterol involvement in the pathogenesis of AD gave epidemiological data of the cholesterol-lowering drugs, statins that have been shown to decrease the risk for AD. This chapter is aimed to summarize existing knowledge about the brain cholesterol metabolism, how the homeostasis is changed during aging and in various neurodegenerative diseases, with special emphasis on Alzheimer’s disease. As a final point, we will try to give a full insight into the environmental influences (including dietary restriction and statins therapy) on brain cholesterol homeostasis.
PB  - Bentham Science Publishers
T2  - Frontiers in Clinical Drug Research-Dementia
T1  - Cholesterol in Brain Health and Pathologies: The Role in Alzheimer’s Disease
DO  - 10.2174/9789811410949120010004
SP  - 26
EP  - 77
ER  - 

@inbook{
editor = "Atta-ur-Rahman",
author = "Smiljanić, Kosara and Lončarević-Vasiljković, Nataša and Kanazir, Selma and Mladenović, Aleksandra",
year = "2020",
abstract = "Cholesterol is the molecule essential for life, but also with a possible detrimental role. Apart from being a vital structural constituent of the cells, cholesterol is a factor involved in many important cell processes. However, it has been known that high blood cholesterol is associated with many pathological conditions. An elevated level of cholesterol is linked with cardiovascular disease, diabetes and neurodegenerative disorders. Almost quarter of the total cholesterol in the body resides in the brain. This vast pool is synthesized in situ and it is almost completely isolated and independent from the periphery due to the presence of blood-brain barrier. In the central nervous system, cholesterol plays important role in neural cells structure and functions, including synaptic transmission. Due to this, its content must be precisely maintained in order to keep brain function well. However, cholesterol is critically challenged in the aging brain and disturbed in several of pathological conditions, like Huntington’s disease (HD), Parkinson’s disease (PD), Niemann-Pick type C (NPC) disease and Smith-Lemli Opitz syndrome (SLOS), traumatic brain injury, multiple sclerosis (MS) and in Alzheimer’s disease (AD). Altered cholesterol metabolism has been extensively implicated in the pathogenesis of AD. A growing amount of evidence underscores the link between disturbed intracellular trafficking of cholesterol in the brain and the formation of amyloid plaques. The inheritance of the epsilon4 allele of the Apolipoprotein E (ApoE), the main transport protein for cholesterol in the brain represents the main risk factor for late onset form of Alzheimer’s disease. Other genetic polymorphisms associated with critical points in cholesterol metabolism may also contribute to the AD pathogenesis. Hypercholesterolemia has been considered nowadays also as a risk factor, and all of these players are thought to promote the production of beta-amyloid and development of AD. Additional proof towards cholesterol involvement in the pathogenesis of AD gave epidemiological data of the cholesterol-lowering drugs, statins that have been shown to decrease the risk for AD. This chapter is aimed to summarize existing knowledge about the brain cholesterol metabolism, how the homeostasis is changed during aging and in various neurodegenerative diseases, with special emphasis on Alzheimer’s disease. As a final point, we will try to give a full insight into the environmental influences (including dietary restriction and statins therapy) on brain cholesterol homeostasis.",
publisher = "Bentham Science Publishers",
journal = "Frontiers in Clinical Drug Research-Dementia",
booktitle = "Cholesterol in Brain Health and Pathologies: The Role in Alzheimer’s Disease",
doi = "10.2174/9789811410949120010004",
pages = "26-77"
}

Atta-ur-Rahman, Smiljanić, K., Lončarević-Vasiljković, N., Kanazir, S.,& Mladenović, A.. (2020). Cholesterol in Brain Health and Pathologies: The Role in Alzheimer’s Disease. in Frontiers in Clinical Drug Research-Dementia
Bentham Science Publishers., 26-77.
https://doi.org/10.2174/9789811410949120010004

Atta-ur-Rahman, Smiljanić K, Lončarević-Vasiljković N, Kanazir S, Mladenović A. Cholesterol in Brain Health and Pathologies: The Role in Alzheimer’s Disease. in Frontiers in Clinical Drug Research-Dementia. 2020;:26-77.
doi:10.2174/9789811410949120010004 .

Atta-ur-Rahman, Smiljanić, Kosara, Lončarević-Vasiljković, Nataša, Kanazir, Selma, Mladenović, Aleksandra, "Cholesterol in Brain Health and Pathologies: The Role in Alzheimer’s Disease" in Frontiers in Clinical Drug Research-Dementia (2020):26-77,
https://doi.org/10.2174/9789811410949120010004 . .

TY  - JOUR
AU  - Todorović, Smilja
AU  - Lončarević-Vasiljković, Nataša
AU  - Jović, Milena
AU  - Sokanović, Srđan
AU  - Kanazir, Selma
AU  - Mladenović, Aleksandra
PY  - 2020
UR  - https://www.sciencedirect.com/science/article/pii/S0047637419302003?via%3Dihub
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3565
AB  - Alzheimer's disease patients (AD), as well as AD transgenic mice, are characterized by increased frailty. Furthermore, the assessment of frailty status represents a feasible approach for detecting individuals prone to develop more severe form of AD and for measuring the outcome of existing and putative AD therapeutics. The 5xFAD mouse is one of the widely used transgenic animal models of AD, but frailty in this model is scantly investigated. We used two validated mouse frailty assessment tools: phenotypic frailty score (FS) and clinical frailty index (FI) to investigate age- and sex- related differences in frailty status in 5xFAD mice. These tools measure different age-related deficits and do not necessarily identify the same subpopulations as frail. We detected a significant increase in frailty with age in both sexes, although females were surprisingly less frail than males. Depending on the tools used, a notable difference in frailty status was detected, with frailty index and frailty score identifying different mice as frail. These results warrant great caution when choosing the frailty tool and point to the need for further adaptation of frailty measurements in mouse models of AD.
PB  - Elsevier
T2  - Mechanisms of Ageing and Development
T1  - Frailty index and phenotype frailty score: Sex- and age-related differences in 5XFAD transgenic mouse model of Alzheimer's disease.
VL  - 185
DO  - 10.1016/j.mad.2019.111195
SP  - 111195
ER  - 

@article{
author = "Todorović, Smilja and Lončarević-Vasiljković, Nataša and Jović, Milena and Sokanović, Srđan and Kanazir, Selma and Mladenović, Aleksandra",
year = "2020",
abstract = "Alzheimer's disease patients (AD), as well as AD transgenic mice, are characterized by increased frailty. Furthermore, the assessment of frailty status represents a feasible approach for detecting individuals prone to develop more severe form of AD and for measuring the outcome of existing and putative AD therapeutics. The 5xFAD mouse is one of the widely used transgenic animal models of AD, but frailty in this model is scantly investigated. We used two validated mouse frailty assessment tools: phenotypic frailty score (FS) and clinical frailty index (FI) to investigate age- and sex- related differences in frailty status in 5xFAD mice. These tools measure different age-related deficits and do not necessarily identify the same subpopulations as frail. We detected a significant increase in frailty with age in both sexes, although females were surprisingly less frail than males. Depending on the tools used, a notable difference in frailty status was detected, with frailty index and frailty score identifying different mice as frail. These results warrant great caution when choosing the frailty tool and point to the need for further adaptation of frailty measurements in mouse models of AD.",
publisher = "Elsevier",
journal = "Mechanisms of Ageing and Development",
title = "Frailty index and phenotype frailty score: Sex- and age-related differences in 5XFAD transgenic mouse model of Alzheimer's disease.",
volume = "185",
doi = "10.1016/j.mad.2019.111195",
pages = "111195"
}

Todorović, S., Lončarević-Vasiljković, N., Jović, M., Sokanović, S., Kanazir, S.,& Mladenović, A.. (2020). Frailty index and phenotype frailty score: Sex- and age-related differences in 5XFAD transgenic mouse model of Alzheimer's disease.. in Mechanisms of Ageing and Development
Elsevier., 185, 111195.
https://doi.org/10.1016/j.mad.2019.111195

Todorović S, Lončarević-Vasiljković N, Jović M, Sokanović S, Kanazir S, Mladenović A. Frailty index and phenotype frailty score: Sex- and age-related differences in 5XFAD transgenic mouse model of Alzheimer's disease.. in Mechanisms of Ageing and Development. 2020;185:111195.
doi:10.1016/j.mad.2019.111195 .

Todorović, Smilja, Lončarević-Vasiljković, Nataša, Jović, Milena, Sokanović, Srđan, Kanazir, Selma, Mladenović, Aleksandra, "Frailty index and phenotype frailty score: Sex- and age-related differences in 5XFAD transgenic mouse model of Alzheimer's disease." in Mechanisms of Ageing and Development, 185 (2020):111195,
https://doi.org/10.1016/j.mad.2019.111195 . .

TY  - JOUR
AU  - Perović, Milka
AU  - Jović, Milena
AU  - Todorović, Smilja
AU  - Mladenović, Aleksandra
AU  - Milanović, Desanka
AU  - Kanazir, Selma
AU  - Lončarević-Vasiljković, Nataša
PY  - 2020
UR  - https://www.tandfonline.com/doi/abs/10.1080/1028415X.2020.1769410
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32476608
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3760
AB  - OBJECTIVE Traumatic brain injury (TBI) is one of the most common causes of neurological damage in young and middle aged people. Food restriction (FR) has been shown to act neuroprotectively in animal models of stroke and TBI. Indeed, our previous studies showed that FR attenuates inflammation, through suppression of microglial activation and TNF-α production, suppresses caspase-3-induced neuronal cell death and enhances neuroplasticity in the rat model of TBI. Glucocorticoids (GCs) play a central role in mediating both molecular and behavioral responses to food restriction. However, the exact mechanisms of FR neuroprotection in TBI are still unclear. The goal of the present study was to examine whether FR exerts its beneficial effects by altering the glucocorticoid receptor (GR) signaling alone and/or together with other protective factors. METHODS To this end, we examined the effects of FR (50% of regular daily food intake for 3 months prior to TBI) on the protein levels of total GR, GR phosphoisoform Ser232 (p-GR) and its transcriptional activity, as well as 11β-HSD1, NFκB (p65) and HSP70 as factors related to the GR signaling. RESULTS Our results demonstrate that FR applied prior to TBI significantly changes p-GR levels, and it's transcriptional activity during the recovery period after TBI. Moreover, as a pretreatment, FR modulates other protective factors in response to TBI, such as 11β-HSD1, NF-κB (p65) and HSP70 that act in parallel with GR in it's anti-inflammatory and neuroprotective effects in the rat model of brain injury. CONCLUSION Our results suggest that prophylactic FR represents a potent non-invasive approach capable of changing GR signalling, together with other factors related to the GR signaling in the model of TBI.
PB  - Taylor and Francis Ltd.
T2  - Nutritional Neuroscience
T1  - Neuroprotective effects of food restriction in a rat model of traumatic brain injury - the role of glucocorticoid signaling.
DO  - 10.1080/1028415X.2020.1769410
ER  - 

@article{
author = "Perović, Milka and Jović, Milena and Todorović, Smilja and Mladenović, Aleksandra and Milanović, Desanka and Kanazir, Selma and Lončarević-Vasiljković, Nataša",
year = "2020",
abstract = "OBJECTIVE Traumatic brain injury (TBI) is one of the most common causes of neurological damage in young and middle aged people. Food restriction (FR) has been shown to act neuroprotectively in animal models of stroke and TBI. Indeed, our previous studies showed that FR attenuates inflammation, through suppression of microglial activation and TNF-α production, suppresses caspase-3-induced neuronal cell death and enhances neuroplasticity in the rat model of TBI. Glucocorticoids (GCs) play a central role in mediating both molecular and behavioral responses to food restriction. However, the exact mechanisms of FR neuroprotection in TBI are still unclear. The goal of the present study was to examine whether FR exerts its beneficial effects by altering the glucocorticoid receptor (GR) signaling alone and/or together with other protective factors. METHODS To this end, we examined the effects of FR (50% of regular daily food intake for 3 months prior to TBI) on the protein levels of total GR, GR phosphoisoform Ser232 (p-GR) and its transcriptional activity, as well as 11β-HSD1, NFκB (p65) and HSP70 as factors related to the GR signaling. RESULTS Our results demonstrate that FR applied prior to TBI significantly changes p-GR levels, and it's transcriptional activity during the recovery period after TBI. Moreover, as a pretreatment, FR modulates other protective factors in response to TBI, such as 11β-HSD1, NF-κB (p65) and HSP70 that act in parallel with GR in it's anti-inflammatory and neuroprotective effects in the rat model of brain injury. CONCLUSION Our results suggest that prophylactic FR represents a potent non-invasive approach capable of changing GR signalling, together with other factors related to the GR signaling in the model of TBI.",
publisher = "Taylor and Francis Ltd.",
journal = "Nutritional Neuroscience",
title = "Neuroprotective effects of food restriction in a rat model of traumatic brain injury - the role of glucocorticoid signaling.",
doi = "10.1080/1028415X.2020.1769410"
}

Perović, M., Jović, M., Todorović, S., Mladenović, A., Milanović, D., Kanazir, S.,& Lončarević-Vasiljković, N.. (2020). Neuroprotective effects of food restriction in a rat model of traumatic brain injury - the role of glucocorticoid signaling.. in Nutritional Neuroscience
Taylor and Francis Ltd...
https://doi.org/10.1080/1028415X.2020.1769410

Perović M, Jović M, Todorović S, Mladenović A, Milanović D, Kanazir S, Lončarević-Vasiljković N. Neuroprotective effects of food restriction in a rat model of traumatic brain injury - the role of glucocorticoid signaling.. in Nutritional Neuroscience. 2020;.
doi:10.1080/1028415X.2020.1769410 .

Perović, Milka, Jović, Milena, Todorović, Smilja, Mladenović, Aleksandra, Milanović, Desanka, Kanazir, Selma, Lončarević-Vasiljković, Nataša, "Neuroprotective effects of food restriction in a rat model of traumatic brain injury - the role of glucocorticoid signaling." in Nutritional Neuroscience (2020),
https://doi.org/10.1080/1028415X.2020.1769410 . .

TY  - CONF
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Ivković, Sanja
AU  - Milanović, Desanka
AU  - Kanazir, Selma
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5803
AB  - Aims: Alzheimer’s disease (AD) is the most prevalent type of dementia in elderly,triggered by multiple factors such as amyloid 
plaques, neurofibrillary tangles and neuroinflammation. The use of supplements with omega-3 fatty acids has been associated 
with reduced risk and lessened AD pathology. The purpose of this study was to elucidate the mechanisms underlying effects of 
short-term fish oil (FO) suplementation in presymptomatic stage of AD in 5xFAD mice.
Methods: Three-month old female 5xFAD mice received FO (100μl/animal/day) via oral gavage during the period of 3 weeks. 
Western blot and immunohistochemical analysis were used to detect changes in pathological features of AD in cortex of 5xFAD 
mice. AmiloGlo was used to visualize plaques. Amyloid beta (Aβ) peptide, dystrophic neurites (DNs), microglia/macrophages 
and CX3CR1/CX3CL1 were detect by anti-Aβ42-, anti-SMI31-, p-Tau-, anti-Iba-1-, anti-CX3CR1 anti-CX3CL1 antibodies, 
retrospectively. Immunostaining was observed by confocal microscopy. Quantification was done by Image J and Image Quant 
softwer. 
Results: The present study shows that short-term FO supplementation applied in presymptomatic stage of AD, alters the 
behaviour of microglia/macrophages prompting them to establish a physical barrier around amyloid plaques. This barrier 
significantly suppresses DNs formation through the reduction of both Aβ content and tau hyperphosphorylation. Moreover, the 
short-term FO treatment suppresses CX3CR1/CX3CL1 axis, interaction between microglial cells and neurons, which represents 
one of possible mechanisms for altered microglial/macrophage motility and colocalization around plaques.
Conclusion: Our findings suggest that FO consumption may play an important role in modulating microglial response and 
ameliorating the AD pathology in presymptomatic stage of Alzheimer’s disease.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
T1  - Mechanism underlying effects of fish oil supplementation in presymptomatic stage of Alzheimer disease in 5XFAD mice
SP  - 287
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5803
ER  - 

@conference{
author = "Jović, Milena and Lončarević-Vasiljković, Nataša and Ivković, Sanja and Milanović, Desanka and Kanazir, Selma",
year = "2019",
abstract = "Aims: Alzheimer’s disease (AD) is the most prevalent type of dementia in elderly,triggered by multiple factors such as amyloid 
plaques, neurofibrillary tangles and neuroinflammation. The use of supplements with omega-3 fatty acids has been associated 
with reduced risk and lessened AD pathology. The purpose of this study was to elucidate the mechanisms underlying effects of 
short-term fish oil (FO) suplementation in presymptomatic stage of AD in 5xFAD mice.
Methods: Three-month old female 5xFAD mice received FO (100μl/animal/day) via oral gavage during the period of 3 weeks. 
Western blot and immunohistochemical analysis were used to detect changes in pathological features of AD in cortex of 5xFAD 
mice. AmiloGlo was used to visualize plaques. Amyloid beta (Aβ) peptide, dystrophic neurites (DNs), microglia/macrophages 
and CX3CR1/CX3CL1 were detect by anti-Aβ42-, anti-SMI31-, p-Tau-, anti-Iba-1-, anti-CX3CR1 anti-CX3CL1 antibodies, 
retrospectively. Immunostaining was observed by confocal microscopy. Quantification was done by Image J and Image Quant 
softwer. 
Results: The present study shows that short-term FO supplementation applied in presymptomatic stage of AD, alters the 
behaviour of microglia/macrophages prompting them to establish a physical barrier around amyloid plaques. This barrier 
significantly suppresses DNs formation through the reduction of both Aβ content and tau hyperphosphorylation. Moreover, the 
short-term FO treatment suppresses CX3CR1/CX3CL1 axis, interaction between microglial cells and neurons, which represents 
one of possible mechanisms for altered microglial/macrophage motility and colocalization around plaques.
Conclusion: Our findings suggest that FO consumption may play an important role in modulating microglial response and 
ameliorating the AD pathology in presymptomatic stage of Alzheimer’s disease.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia",
title = "Mechanism underlying effects of fish oil supplementation in presymptomatic stage of Alzheimer disease in 5XFAD mice",
pages = "287",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5803"
}

Jović, M., Lončarević-Vasiljković, N., Ivković, S., Milanović, D.,& Kanazir, S.. (2019). Mechanism underlying effects of fish oil supplementation in presymptomatic stage of Alzheimer disease in 5XFAD mice. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 287.
https://hdl.handle.net/21.15107/rcub_ibiss_5803

Jović M, Lončarević-Vasiljković N, Ivković S, Milanović D, Kanazir S. Mechanism underlying effects of fish oil supplementation in presymptomatic stage of Alzheimer disease in 5XFAD mice. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia. 2019;:287.
https://hdl.handle.net/21.15107/rcub_ibiss_5803 .

Jović, Milena, Lončarević-Vasiljković, Nataša, Ivković, Sanja, Milanović, Desanka, Kanazir, Selma, "Mechanism underlying effects of fish oil supplementation in presymptomatic stage of Alzheimer disease in 5XFAD mice" in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia (2019):287,
https://hdl.handle.net/21.15107/rcub_ibiss_5803 .

TY  - JOUR
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Ivković, Sanja
AU  - Dinić, Jelena
AU  - Milanović, Desanka
AU  - Zloković, Berislav
AU  - Kanazir, Selma
PY  - 2019
UR  - http://dx.plos.org/10.1371/journal.pone.0216726
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC6522015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3405
AB  - Dystrophic neurites and activated microglia are one of the main neuropathological characteristics of Alzheimer's disease (AD). Although the use of supplements with omega-3 fatty acids has been associated with reduced risk and lessened AD pathology, it still remains elusive whether such a treatment could affect dystrophic neurites (DNs) formation and microglia/macrophage behavior in the early phase of disease. We analyzed the effects of short-term (3 weeks) fish oil supplementation on DNs formation, tau hyperphosphorylation, Amyloid-beta peptide 1-42 (Aβ42) levels and microglial/macrophage response to AD pathology in the parietal cortex of 4-month-old 5xFAD mice, a mouse model of AD. The present study shows for the first time that short-term FO supplementation applied in presymptomatic stage of AD, alters the behaviour of microglia/macrophages prompting them to establish a physical barrier around amyloid plaques. This barrier significantly suppresses DNs formation through the reduction of both Aβ content and tau hyperphosphorylation. Moreover, the short-term FO treatment neither suppresses inflammation nor enhances phagocytic properties of microglia/macrophages in the response to Aβ pathology, the effects most commonly attributed to the fish oil supplementation. Our findings suggest that fish oil consumption may play an important role in modulating microglial/macrophage response and ameliorating the AD pathology in presymptomatic stage of Alzheimer's disease.
T2  - PloS One
T1  - Short-term fish oil supplementation applied in presymptomatic stage of Alzheimer's disease enhances microglial/macrophage barrier and prevents neuritic dystrophy in parietal cortex of 5xFAD mouse model.
IS  - 5
VL  - 14
DO  - 10.1371/journal.pone.0216726
SP  - e0216726
ER  - 

@article{
author = "Jović, Milena and Lončarević-Vasiljković, Nataša and Ivković, Sanja and Dinić, Jelena and Milanović, Desanka and Zloković, Berislav and Kanazir, Selma",
year = "2019",
abstract = "Dystrophic neurites and activated microglia are one of the main neuropathological characteristics of Alzheimer's disease (AD). Although the use of supplements with omega-3 fatty acids has been associated with reduced risk and lessened AD pathology, it still remains elusive whether such a treatment could affect dystrophic neurites (DNs) formation and microglia/macrophage behavior in the early phase of disease. We analyzed the effects of short-term (3 weeks) fish oil supplementation on DNs formation, tau hyperphosphorylation, Amyloid-beta peptide 1-42 (Aβ42) levels and microglial/macrophage response to AD pathology in the parietal cortex of 4-month-old 5xFAD mice, a mouse model of AD. The present study shows for the first time that short-term FO supplementation applied in presymptomatic stage of AD, alters the behaviour of microglia/macrophages prompting them to establish a physical barrier around amyloid plaques. This barrier significantly suppresses DNs formation through the reduction of both Aβ content and tau hyperphosphorylation. Moreover, the short-term FO treatment neither suppresses inflammation nor enhances phagocytic properties of microglia/macrophages in the response to Aβ pathology, the effects most commonly attributed to the fish oil supplementation. Our findings suggest that fish oil consumption may play an important role in modulating microglial/macrophage response and ameliorating the AD pathology in presymptomatic stage of Alzheimer's disease.",
journal = "PloS One",
title = "Short-term fish oil supplementation applied in presymptomatic stage of Alzheimer's disease enhances microglial/macrophage barrier and prevents neuritic dystrophy in parietal cortex of 5xFAD mouse model.",
number = "5",
volume = "14",
doi = "10.1371/journal.pone.0216726",
pages = "e0216726"
}

Jović, M., Lončarević-Vasiljković, N., Ivković, S., Dinić, J., Milanović, D., Zloković, B.,& Kanazir, S.. (2019). Short-term fish oil supplementation applied in presymptomatic stage of Alzheimer's disease enhances microglial/macrophage barrier and prevents neuritic dystrophy in parietal cortex of 5xFAD mouse model.. in PloS One, 14(5), e0216726.
https://doi.org/10.1371/journal.pone.0216726

Jović M, Lončarević-Vasiljković N, Ivković S, Dinić J, Milanović D, Zloković B, Kanazir S. Short-term fish oil supplementation applied in presymptomatic stage of Alzheimer's disease enhances microglial/macrophage barrier and prevents neuritic dystrophy in parietal cortex of 5xFAD mouse model.. in PloS One. 2019;14(5):e0216726.
doi:10.1371/journal.pone.0216726 .

Jović, Milena, Lončarević-Vasiljković, Nataša, Ivković, Sanja, Dinić, Jelena, Milanović, Desanka, Zloković, Berislav, Kanazir, Selma, "Short-term fish oil supplementation applied in presymptomatic stage of Alzheimer's disease enhances microglial/macrophage barrier and prevents neuritic dystrophy in parietal cortex of 5xFAD mouse model." in PloS One, 14, no. 5 (2019):e0216726,
https://doi.org/10.1371/journal.pone.0216726 . .

TY  - CONF
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Ivković, Sanja
AU  - Milanović, Desanka
AU  - Avramović, Vladimir
AU  - Kanazir, Selma
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5719
AB  - Defining features of Alzheimer's disease (AD) pathology are the formation of amyloid plaques, neurofibrillary tangles, neuron loss and inflammation. Plaques are encircled by a halo of diffuse Aβ, surrounded by dystrophic neurites (DNs) and activated glia. High level of Aβ suppresses microglial ability to clear Aβ and activate inflammatory response that becomes neurotoxic. These microglial cells become dysfunctional and can further contribute to AD pathology. 

We investigated the influence of omega-3 fatty acids, the main compounds of fish oil (FO), on Aβ load, neuritic dystrophy and behavior of microglial cells in parietal cortex in 5xFAD mice. 

Three-month old female 5xFAD mice received FO (100μl/animal/day) via oral gavage during 3 weeks period. Aβ-pathology was visualized immunohistochemically. We used ThioflavinS and AmiloGlo to visualize plaques, anti-Aβ42 antibody for soluble Aβ peptide labeling, anti-SMI31 antibody for neuritic dystrophy and anti-Iba-1 antibody for microglial cells. Immunostaining was observed by confocal microscopy. Quantification was done by Image J program. 

Our results showed that short-term FO supplementation was capable of: (i) inducing significant decreased of total Aβ levels (ii) preventing the emergence of neuritic dystrophy in parietal cortex of 5xFAD mice; (iii) increasing overall microglial number; and (iv) enhancing clustering of microglial cells around amyloid plaques, representing mechanical barrier that prevents further Aβ  aggregation. 

This study represents valuable contribution to better biological understanding how FO suppresses AD pathology through typical pleiotropic effect. We believe that FO in combination with other drugs could be good approach for long-term treatment in slowing down AD pathology.
PB  - Brussels, Belgium: Federation of European Neurocience Societies
C3  - 11th FENS Forum of Neuroscience; 2018 Jul 7-11; Berlin, Germany
T1  - Influence of fish oil treatment on microglial cell behavior and Aβ-like pathology in 5xFAD mice model of Alzheimer’s disease
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5719
ER  - 

@conference{
author = "Jović, Milena and Lončarević-Vasiljković, Nataša and Ivković, Sanja and Milanović, Desanka and Avramović, Vladimir and Kanazir, Selma",
year = "2018",
abstract = "Defining features of Alzheimer's disease (AD) pathology are the formation of amyloid plaques, neurofibrillary tangles, neuron loss and inflammation. Plaques are encircled by a halo of diffuse Aβ, surrounded by dystrophic neurites (DNs) and activated glia. High level of Aβ suppresses microglial ability to clear Aβ and activate inflammatory response that becomes neurotoxic. These microglial cells become dysfunctional and can further contribute to AD pathology. 

We investigated the influence of omega-3 fatty acids, the main compounds of fish oil (FO), on Aβ load, neuritic dystrophy and behavior of microglial cells in parietal cortex in 5xFAD mice. 

Three-month old female 5xFAD mice received FO (100μl/animal/day) via oral gavage during 3 weeks period. Aβ-pathology was visualized immunohistochemically. We used ThioflavinS and AmiloGlo to visualize plaques, anti-Aβ42 antibody for soluble Aβ peptide labeling, anti-SMI31 antibody for neuritic dystrophy and anti-Iba-1 antibody for microglial cells. Immunostaining was observed by confocal microscopy. Quantification was done by Image J program. 

Our results showed that short-term FO supplementation was capable of: (i) inducing significant decreased of total Aβ levels (ii) preventing the emergence of neuritic dystrophy in parietal cortex of 5xFAD mice; (iii) increasing overall microglial number; and (iv) enhancing clustering of microglial cells around amyloid plaques, representing mechanical barrier that prevents further Aβ  aggregation. 

This study represents valuable contribution to better biological understanding how FO suppresses AD pathology through typical pleiotropic effect. We believe that FO in combination with other drugs could be good approach for long-term treatment in slowing down AD pathology.",
publisher = "Brussels, Belgium: Federation of European Neurocience Societies",
journal = "11th FENS Forum of Neuroscience; 2018 Jul 7-11; Berlin, Germany",
title = "Influence of fish oil treatment on microglial cell behavior and Aβ-like pathology in 5xFAD mice model of Alzheimer’s disease",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5719"
}

Jović, M., Lončarević-Vasiljković, N., Ivković, S., Milanović, D., Avramović, V.,& Kanazir, S.. (2018). Influence of fish oil treatment on microglial cell behavior and Aβ-like pathology in 5xFAD mice model of Alzheimer’s disease. in 11th FENS Forum of Neuroscience; 2018 Jul 7-11; Berlin, Germany
Brussels, Belgium: Federation of European Neurocience Societies..
https://hdl.handle.net/21.15107/rcub_ibiss_5719

Jović M, Lončarević-Vasiljković N, Ivković S, Milanović D, Avramović V, Kanazir S. Influence of fish oil treatment on microglial cell behavior and Aβ-like pathology in 5xFAD mice model of Alzheimer’s disease. in 11th FENS Forum of Neuroscience; 2018 Jul 7-11; Berlin, Germany. 2018;.
https://hdl.handle.net/21.15107/rcub_ibiss_5719 .

Jović, Milena, Lončarević-Vasiljković, Nataša, Ivković, Sanja, Milanović, Desanka, Avramović, Vladimir, Kanazir, Selma, "Influence of fish oil treatment on microglial cell behavior and Aβ-like pathology in 5xFAD mice model of Alzheimer’s disease" in 11th FENS Forum of Neuroscience; 2018 Jul 7-11; Berlin, Germany (2018),
https://hdl.handle.net/21.15107/rcub_ibiss_5719 .

TY  - CONF
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Ivković, Sanja
AU  - Milanović, Desanka
AU  - Avramović, Vladimir
AU  - Kanazir, Selma
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5716
AB  - Dystrophic neurites (DNs) and activated microglia are one of the neuropathological characteristics of Alzheimer's disease (AD). Although the use of supplements with omega-3 (0) fatty acids has been associated with reduced risk and lessened. AD pathology, it still remains elusive whether such a treatment could affect DNs formation and microglia behavior in the early phase of disease. We examined influence of fish oil treatment on pathological hallmarks in the brain of 5xFAD mice which rapidly recapitulate major hallmarks of AD amyloid pathology. Three-month old female 5xFAD mice received FO (10011.1/animal/day) via oral Savage during 3 weeks period. Histological analysis was used to detect changes in pathological features of AD in parietal cortex in 5xFAD mice. ThioflavinS and AmiloGlo were used to visualize plaques. Soluble Ap peptide, neuritic dystrophy and microglial cells were detect by anti-A1342-, anti-SMI31- and anti-Iba-1- antibodies, retrospectively. Immunostaining was observed by confocal microscopy. Quantification was done by Image J program. Our results showed that short-term FO supplementation is capable of inducing significant decreased of total Ap levels and preventing the emergence of neuritic dystrophy in parietal cortex of 5xFAD mice. FO supplementation led to increase in overall microglial number and enhanced clustering of microglial cells around amyloid plaques, representing mechanical barrier that doesn't allow AP to aggregate. These results confirmed and extended previous findings suggesting that FO suppresses brain aging and has a typical pleiotropic effect. We believe that FO in combination with other drugs could be good approach for long-term treatment in AD suppression.
PB  - FEBS Balaton 2018
C3  - Final Programme and Book of Abstracts: FEBS3+: From molecules to living systems; 2018 Sep 2-5; Siofok, Hungary
T1  - Influence of fish oil treatment on microglial cell behavior and dystrophic neurites in 5XFAD mice model of Alzheimer's disease
SP  - P8-03
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5716
ER  - 

@conference{
author = "Jović, Milena and Lončarević-Vasiljković, Nataša and Ivković, Sanja and Milanović, Desanka and Avramović, Vladimir and Kanazir, Selma",
year = "2018",
abstract = "Dystrophic neurites (DNs) and activated microglia are one of the neuropathological characteristics of Alzheimer's disease (AD). Although the use of supplements with omega-3 (0) fatty acids has been associated with reduced risk and lessened. AD pathology, it still remains elusive whether such a treatment could affect DNs formation and microglia behavior in the early phase of disease. We examined influence of fish oil treatment on pathological hallmarks in the brain of 5xFAD mice which rapidly recapitulate major hallmarks of AD amyloid pathology. Three-month old female 5xFAD mice received FO (10011.1/animal/day) via oral Savage during 3 weeks period. Histological analysis was used to detect changes in pathological features of AD in parietal cortex in 5xFAD mice. ThioflavinS and AmiloGlo were used to visualize plaques. Soluble Ap peptide, neuritic dystrophy and microglial cells were detect by anti-A1342-, anti-SMI31- and anti-Iba-1- antibodies, retrospectively. Immunostaining was observed by confocal microscopy. Quantification was done by Image J program. Our results showed that short-term FO supplementation is capable of inducing significant decreased of total Ap levels and preventing the emergence of neuritic dystrophy in parietal cortex of 5xFAD mice. FO supplementation led to increase in overall microglial number and enhanced clustering of microglial cells around amyloid plaques, representing mechanical barrier that doesn't allow AP to aggregate. These results confirmed and extended previous findings suggesting that FO suppresses brain aging and has a typical pleiotropic effect. We believe that FO in combination with other drugs could be good approach for long-term treatment in AD suppression.",
publisher = "FEBS Balaton 2018",
journal = "Final Programme and Book of Abstracts: FEBS3+: From molecules to living systems; 2018 Sep 2-5; Siofok, Hungary",
title = "Influence of fish oil treatment on microglial cell behavior and dystrophic neurites in 5XFAD mice model of Alzheimer's disease",
pages = "P8-03",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5716"
}

Jović, M., Lončarević-Vasiljković, N., Ivković, S., Milanović, D., Avramović, V.,& Kanazir, S.. (2018). Influence of fish oil treatment on microglial cell behavior and dystrophic neurites in 5XFAD mice model of Alzheimer's disease. in Final Programme and Book of Abstracts: FEBS3+: From molecules to living systems; 2018 Sep 2-5; Siofok, Hungary
FEBS Balaton 2018., P8-03.
https://hdl.handle.net/21.15107/rcub_ibiss_5716

Jović M, Lončarević-Vasiljković N, Ivković S, Milanović D, Avramović V, Kanazir S. Influence of fish oil treatment on microglial cell behavior and dystrophic neurites in 5XFAD mice model of Alzheimer's disease. in Final Programme and Book of Abstracts: FEBS3+: From molecules to living systems; 2018 Sep 2-5; Siofok, Hungary. 2018;:P8-03.
https://hdl.handle.net/21.15107/rcub_ibiss_5716 .

Jović, Milena, Lončarević-Vasiljković, Nataša, Ivković, Sanja, Milanović, Desanka, Avramović, Vladimir, Kanazir, Selma, "Influence of fish oil treatment on microglial cell behavior and dystrophic neurites in 5XFAD mice model of Alzheimer's disease" in Final Programme and Book of Abstracts: FEBS3+: From molecules to living systems; 2018 Sep 2-5; Siofok, Hungary (2018):P8-03,
https://hdl.handle.net/21.15107/rcub_ibiss_5716 .

TY  - JOUR
AU  - Milanović, Desanka
AU  - Pešić, Vesna
AU  - Lončarević-Vasiljković, Nataša
AU  - Avramović, Vladimir
AU  - Tešić, Vesna
AU  - Jevtović-Todorović, Vesna
AU  - Kanazir, Selma
AU  - Ruždijić, Sabera
PY  - 2017
UR  - http://link.springer.com/10.1007/s12640-017-9730-0
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2741
AB  - Propofol is a general anesthetic commonly used in pediatric clinical practices. Experimental findings demonstrate that anesthetics induce widespread apoptosis and cognitive decline in a developing brain. Although anesthesia-mediated neurotoxicity is the most prominent during intense period of synaptogenesis, the effects of an early anesthesia exposure on the synapses are not well understood. The aim of this study was to examine the effects of neonatal propofol anesthesia on the expression of key proteins that participate in synaptogenesis and synaptic plasticity and to evaluate long-term neurobehavioral abnormalities in the mature adult brain. Propofol-injected 7-day-old rats were maintained under 2-, 4-, and 6-h-long anesthesia and sacrificed 0, 4, 16, and 24 h after the termination of each exposure. We showed that propofol anesthesia strongly influenced spatiotemporal expression and/or proteolytic processing of crucial presynaptic (GAP-43, synaptophysin, α-synuclein), trans-synaptic (N-cadherin), and postsynaptic (drebrin, MAP-2) proteins in the cortex and thalamus. An overall decrease of synaptophysin, α-synuclein, N-cadherin, and drebrin indicated impaired function and structure of the synaptic contacts immediately after anesthesia cessation. GAP-43 and MAP-2 adult and juvenile isoforms are upregulated following anesthesia, suggesting compensatory mechanism in the maintaining of the structural integrity and stabilization of developing axons and dendritic arbors. Neonatal propofol exposure significantly altered spontaneous motor activity (increased stereotypic/repetitive movements) and changed emotional behavior (reduced anxiety-like response) in the adulthood, 6 months later. These findings suggest that propofol anesthesia is synaptotoxic in the developing brain, disturbing synaptic dynamics and producing neuroplastic changes permanently incorporated into existing networks with long-lasting functional consequences.
T2  - Neurotoxicity Research
T1  - Neonatal Propofol Anesthesia Changes Expression of Synaptic Plasticity Proteins and Increases Stereotypic and Anxyolitic Behavior in Adult Rats
VL  - 32
DO  - 10.1007/s12640-017-9730-0
SP  - 247
EP  - 263
ER  - 

@article{
author = "Milanović, Desanka and Pešić, Vesna and Lončarević-Vasiljković, Nataša and Avramović, Vladimir and Tešić, Vesna and Jevtović-Todorović, Vesna and Kanazir, Selma and Ruždijić, Sabera",
year = "2017",
abstract = "Propofol is a general anesthetic commonly used in pediatric clinical practices. Experimental findings demonstrate that anesthetics induce widespread apoptosis and cognitive decline in a developing brain. Although anesthesia-mediated neurotoxicity is the most prominent during intense period of synaptogenesis, the effects of an early anesthesia exposure on the synapses are not well understood. The aim of this study was to examine the effects of neonatal propofol anesthesia on the expression of key proteins that participate in synaptogenesis and synaptic plasticity and to evaluate long-term neurobehavioral abnormalities in the mature adult brain. Propofol-injected 7-day-old rats were maintained under 2-, 4-, and 6-h-long anesthesia and sacrificed 0, 4, 16, and 24 h after the termination of each exposure. We showed that propofol anesthesia strongly influenced spatiotemporal expression and/or proteolytic processing of crucial presynaptic (GAP-43, synaptophysin, α-synuclein), trans-synaptic (N-cadherin), and postsynaptic (drebrin, MAP-2) proteins in the cortex and thalamus. An overall decrease of synaptophysin, α-synuclein, N-cadherin, and drebrin indicated impaired function and structure of the synaptic contacts immediately after anesthesia cessation. GAP-43 and MAP-2 adult and juvenile isoforms are upregulated following anesthesia, suggesting compensatory mechanism in the maintaining of the structural integrity and stabilization of developing axons and dendritic arbors. Neonatal propofol exposure significantly altered spontaneous motor activity (increased stereotypic/repetitive movements) and changed emotional behavior (reduced anxiety-like response) in the adulthood, 6 months later. These findings suggest that propofol anesthesia is synaptotoxic in the developing brain, disturbing synaptic dynamics and producing neuroplastic changes permanently incorporated into existing networks with long-lasting functional consequences.",
journal = "Neurotoxicity Research",
title = "Neonatal Propofol Anesthesia Changes Expression of Synaptic Plasticity Proteins and Increases Stereotypic and Anxyolitic Behavior in Adult Rats",
volume = "32",
doi = "10.1007/s12640-017-9730-0",
pages = "247-263"
}

Milanović, D., Pešić, V., Lončarević-Vasiljković, N., Avramović, V., Tešić, V., Jevtović-Todorović, V., Kanazir, S.,& Ruždijić, S.. (2017). Neonatal Propofol Anesthesia Changes Expression of Synaptic Plasticity Proteins and Increases Stereotypic and Anxyolitic Behavior in Adult Rats. in Neurotoxicity Research, 32, 247-263.
https://doi.org/10.1007/s12640-017-9730-0

Milanović D, Pešić V, Lončarević-Vasiljković N, Avramović V, Tešić V, Jevtović-Todorović V, Kanazir S, Ruždijić S. Neonatal Propofol Anesthesia Changes Expression of Synaptic Plasticity Proteins and Increases Stereotypic and Anxyolitic Behavior in Adult Rats. in Neurotoxicity Research. 2017;32:247-263.
doi:10.1007/s12640-017-9730-0 .

Milanović, Desanka, Pešić, Vesna, Lončarević-Vasiljković, Nataša, Avramović, Vladimir, Tešić, Vesna, Jevtović-Todorović, Vesna, Kanazir, Selma, Ruždijić, Sabera, "Neonatal Propofol Anesthesia Changes Expression of Synaptic Plasticity Proteins and Increases Stereotypic and Anxyolitic Behavior in Adult Rats" in Neurotoxicity Research, 32 (2017):247-263,
https://doi.org/10.1007/s12640-017-9730-0 . .

TY  - CONF
AU  - Lončarević-Vasiljković, Nataša
AU  - Jović, Milena
AU  - Ivković, Sanja
AU  - Milanović, Desanka
AU  - Dinić, Jelena
AU  - Brkić, Marjana
AU  - Avramović, Vladimir
AU  - Kanazir, Selma
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6001
AB  - Introduction. Dystrophic neurites (DNs) are one of the neuropathological characteristics of Alzheimer's disease (AD) and represent the initial phase of neurodegeneration. Microtubule disruption in presynaptic dystrophic neurites that surround plaques impairs axonal transport and leads to the exacerbation of amyloid pathology in AD. Microglia plays a pivotal role in AD pathology as it is able to constitute a physical barrier around amyloid plaques and limit the accumulation of protofibrilar amyloid beta around the fibrillar plaque core. In such a way microglia can mechanically shield the surrounding neurites from the neurotoxic protofibrillar Aβ aggregates. The use of supplements with omega-3 (ω3) fatty acids (FAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), such as fish oil, is widespread due to proposed beneficial effects on the nervous system. High DHA consumption has been also associated with reduced risk and lessened AD pathology, yet the mechanisms and therapeutic potential  of these supplements remain elusive. Material and Methods. We analyzed the effects of the short-term fish oil (FO) supplementation on 4 months old 5xFAD mice, a mouse model with fast and robust development of the AD pathology hallmarks such as amyloid plaques and dystrophic neurites. Results. We  showed that even the short treatment with FO can affect the microglia clustering around amyloid plaques and increase the microglial plaque envelopment. Consequently, the Aβ accumulation was reduced and the appearance of DNs substantially suppressed. Conclusion. Our findings suggest that increased DHA consumption may play and important role in modulating microglial response and ameliorating AD pathology at least in the early phase of the disease.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
T1  - The newly discovered effects of fish oil supplementation on AD pathology: What’s next?
SP  - 33
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6001
ER  - 

@conference{
author = "Lončarević-Vasiljković, Nataša and Jović, Milena and Ivković, Sanja and Milanović, Desanka and Dinić, Jelena and Brkić, Marjana and Avramović, Vladimir and Kanazir, Selma",
year = "2017",
abstract = "Introduction. Dystrophic neurites (DNs) are one of the neuropathological characteristics of Alzheimer's disease (AD) and represent the initial phase of neurodegeneration. Microtubule disruption in presynaptic dystrophic neurites that surround plaques impairs axonal transport and leads to the exacerbation of amyloid pathology in AD. Microglia plays a pivotal role in AD pathology as it is able to constitute a physical barrier around amyloid plaques and limit the accumulation of protofibrilar amyloid beta around the fibrillar plaque core. In such a way microglia can mechanically shield the surrounding neurites from the neurotoxic protofibrillar Aβ aggregates. The use of supplements with omega-3 (ω3) fatty acids (FAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), such as fish oil, is widespread due to proposed beneficial effects on the nervous system. High DHA consumption has been also associated with reduced risk and lessened AD pathology, yet the mechanisms and therapeutic potential  of these supplements remain elusive. Material and Methods. We analyzed the effects of the short-term fish oil (FO) supplementation on 4 months old 5xFAD mice, a mouse model with fast and robust development of the AD pathology hallmarks such as amyloid plaques and dystrophic neurites. Results. We  showed that even the short treatment with FO can affect the microglia clustering around amyloid plaques and increase the microglial plaque envelopment. Consequently, the Aβ accumulation was reduced and the appearance of DNs substantially suppressed. Conclusion. Our findings suggest that increased DHA consumption may play and important role in modulating microglial response and ameliorating AD pathology at least in the early phase of the disease.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia",
title = "The newly discovered effects of fish oil supplementation on AD pathology: What’s next?",
pages = "33",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6001"
}

Lončarević-Vasiljković, N., Jović, M., Ivković, S., Milanović, D., Dinić, J., Brkić, M., Avramović, V.,& Kanazir, S.. (2017). The newly discovered effects of fish oil supplementation on AD pathology: What’s next?. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 33.
https://hdl.handle.net/21.15107/rcub_ibiss_6001

Lončarević-Vasiljković N, Jović M, Ivković S, Milanović D, Dinić J, Brkić M, Avramović V, Kanazir S. The newly discovered effects of fish oil supplementation on AD pathology: What’s next?. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia. 2017;:33.
https://hdl.handle.net/21.15107/rcub_ibiss_6001 .

Lončarević-Vasiljković, Nataša, Jović, Milena, Ivković, Sanja, Milanović, Desanka, Dinić, Jelena, Brkić, Marjana, Avramović, Vladimir, Kanazir, Selma, "The newly discovered effects of fish oil supplementation on AD pathology: What’s next?" in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia (2017):33,
https://hdl.handle.net/21.15107/rcub_ibiss_6001 .

TY  - CONF
AU  - Mladenović, Aleksandra
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Athanasopoulou, Sofia
AU  - Gonos, Efstathios S
AU  - Kanazir, Selma
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5809
AB  - Introduction. Aging represents the most important risk factor for Alzheimer’s
disease (AD), the most common neurodegenerative disorders worldwide. One of 
the hallmarks of AD is the accumulation of plaques composed of aggregated 
amyloid-β peptides (Aβ) which are formed by sequential proteolytic processing 
of the amyloid-precursor protein (APP).It is well known that different factors 
can influence amyloidogenic pathway and/or clearance of already formed Aβ. 
Growing evidence suggest that ubiquitin proteasomal system represents an 
important factor in AD development and a potential target for the management 
of disease. Recently it has been shown that several natural compounds, 
including 18α-glycyrrhetinic acid (18α-GA) protects from protein aggregation related pathology in AD model system. Methods. In order to investigate the 
protective effect of 18α-GA, we used 5xFAD transgenic mouse AD model, 
characterized by early amyloid deposition and intra-neuronal Aβ42 aggregation. 
Both female and male mice were exposed to 18α-GA treatment for one month, 
started at 2-months of age. This is considered as an early phase of AD pathology, 
known to be suitable for therapeutics application. In the cortex and 
hippocampus CT-L, T-L, and PGPH proteasome activities were assayed by 
hydrolysis of Suc-LLVY-AMC, Boc-LRR-AMC, and Z-LLE-AMC fluorogenic 
peptides. The number and size of amyloid plaques were determined in these 
structures. Results. This study revealed that 18α-GA treatment influence 
neuritic dystrophy, increase proteasome activity, decrease Aβ content and 
number of amyloid plaques in 5xFAD mice. Conclusion. These preliminary 
intriguing data open up new directions using natural compounds for the most 
efficient treatment of neurodegenerative disorders.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
T1  - Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease
SP  - 109
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5809
ER  - 

@conference{
author = "Mladenović, Aleksandra and Jović, Milena and Lončarević-Vasiljković, Nataša and Athanasopoulou, Sofia and Gonos, Efstathios S and Kanazir, Selma",
year = "2017",
abstract = "Introduction. Aging represents the most important risk factor for Alzheimer’s
disease (AD), the most common neurodegenerative disorders worldwide. One of 
the hallmarks of AD is the accumulation of plaques composed of aggregated 
amyloid-β peptides (Aβ) which are formed by sequential proteolytic processing 
of the amyloid-precursor protein (APP).It is well known that different factors 
can influence amyloidogenic pathway and/or clearance of already formed Aβ. 
Growing evidence suggest that ubiquitin proteasomal system represents an 
important factor in AD development and a potential target for the management 
of disease. Recently it has been shown that several natural compounds, 
including 18α-glycyrrhetinic acid (18α-GA) protects from protein aggregation related pathology in AD model system. Methods. In order to investigate the 
protective effect of 18α-GA, we used 5xFAD transgenic mouse AD model, 
characterized by early amyloid deposition and intra-neuronal Aβ42 aggregation. 
Both female and male mice were exposed to 18α-GA treatment for one month, 
started at 2-months of age. This is considered as an early phase of AD pathology, 
known to be suitable for therapeutics application. In the cortex and 
hippocampus CT-L, T-L, and PGPH proteasome activities were assayed by 
hydrolysis of Suc-LLVY-AMC, Boc-LRR-AMC, and Z-LLE-AMC fluorogenic 
peptides. The number and size of amyloid plaques were determined in these 
structures. Results. This study revealed that 18α-GA treatment influence 
neuritic dystrophy, increase proteasome activity, decrease Aβ content and 
number of amyloid plaques in 5xFAD mice. Conclusion. These preliminary 
intriguing data open up new directions using natural compounds for the most 
efficient treatment of neurodegenerative disorders.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia",
title = "Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease",
pages = "109",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5809"
}

Mladenović, A., Jović, M., Lončarević-Vasiljković, N., Athanasopoulou, S., Gonos, E. S.,& Kanazir, S.. (2017). Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 109.
https://hdl.handle.net/21.15107/rcub_ibiss_5809

Mladenović A, Jović M, Lončarević-Vasiljković N, Athanasopoulou S, Gonos ES, Kanazir S. Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia. 2017;:109.
https://hdl.handle.net/21.15107/rcub_ibiss_5809 .

Mladenović, Aleksandra, Jović, Milena, Lončarević-Vasiljković, Nataša, Athanasopoulou, Sofia, Gonos, Efstathios S, Kanazir, Selma, "Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease" in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia (2017):109,
https://hdl.handle.net/21.15107/rcub_ibiss_5809 .

TY  - CONF
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Avramović, Vladimir
AU  - Brkić, Marjana
AU  - Milanović, Desanka
AU  - Kanazir, Selma
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5804
AB  - Introduction: Alzheimer's disease (AD) is the most prevalent neurodegenerative 
disease in elderly. Defining feature of AD pathology is the formation of amyloid 
plaques, structures that are composed of fibrillar Amyloid-β organized in a β-sheet 
conformation. In AD pathology the clinical symptoms mirror the pathological 
changes in the brain, where the neuronal loss and plaque pathology occur in the 
memory related areas. The onset of neuritic dystrophy represents the initial phase of 
neurodegeneration. It occurs in an early phase of pathology called latent phase, 
which leaves time frame for potential treatments. So far, omega 3 fatty acids 
(omega-3 FA), one of the main compounds of fish oil (FO), represent one of the most 
promising treatment. Here we investigated influence of omega-3 FA 
supplementation on number of plaques, Aβ load and neuritic dystrophy in parietal 
cortex in 5XFAD mice.
Methods: Three-month old female 5xFAD mice received FO (100 μl/animal/day) via 
oral gavage during a 3-week period. Number of plaques, total Aβ levels and neuritic 
dystrophy were visualized by immunohistochemistry and quantification was done by 
Image J software.
Results: Our results showed that 3 weeks of FO supplementation significantly 
decreased number of plaques, total Aβ levels and neuritic dystrophy in the parietal 
cortex of FO-supplemented 5xFAD animals as compared to non-supplemented 
5xFAD animals.
Conclusion: Since fish oil supplementation proved to be able to stop neuritic 
dystrophy in the parietal cortex of 5xFAD mice it may represent good approach for 
long term treatment in AD prevention.
PB  - Belgrade: University of Belgrade, Faculty of Biology
C3  - Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
T1  - Fish oil supplementation suppress neuritic dystrophy and Аβ pathology in parietal cortex of 5XFAD mice
SP  - 45
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5804
ER  - 

@conference{
author = "Jović, Milena and Lončarević-Vasiljković, Nataša and Avramović, Vladimir and Brkić, Marjana and Milanović, Desanka and Kanazir, Selma",
year = "2017",
abstract = "Introduction: Alzheimer's disease (AD) is the most prevalent neurodegenerative 
disease in elderly. Defining feature of AD pathology is the formation of amyloid 
plaques, structures that are composed of fibrillar Amyloid-β organized in a β-sheet 
conformation. In AD pathology the clinical symptoms mirror the pathological 
changes in the brain, where the neuronal loss and plaque pathology occur in the 
memory related areas. The onset of neuritic dystrophy represents the initial phase of 
neurodegeneration. It occurs in an early phase of pathology called latent phase, 
which leaves time frame for potential treatments. So far, omega 3 fatty acids 
(omega-3 FA), one of the main compounds of fish oil (FO), represent one of the most 
promising treatment. Here we investigated influence of omega-3 FA 
supplementation on number of plaques, Aβ load and neuritic dystrophy in parietal 
cortex in 5XFAD mice.
Methods: Three-month old female 5xFAD mice received FO (100 μl/animal/day) via 
oral gavage during a 3-week period. Number of plaques, total Aβ levels and neuritic 
dystrophy were visualized by immunohistochemistry and quantification was done by 
Image J software.
Results: Our results showed that 3 weeks of FO supplementation significantly 
decreased number of plaques, total Aβ levels and neuritic dystrophy in the parietal 
cortex of FO-supplemented 5xFAD animals as compared to non-supplemented 
5xFAD animals.
Conclusion: Since fish oil supplementation proved to be able to stop neuritic 
dystrophy in the parietal cortex of 5xFAD mice it may represent good approach for 
long term treatment in AD prevention.",
publisher = "Belgrade: University of Belgrade, Faculty of Biology",
journal = "Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.",
title = "Fish oil supplementation suppress neuritic dystrophy and Аβ pathology in parietal cortex of 5XFAD mice",
pages = "45",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5804"
}

Jović, M., Lončarević-Vasiljković, N., Avramović, V., Brkić, M., Milanović, D.,& Kanazir, S.. (2017). Fish oil supplementation suppress neuritic dystrophy and Аβ pathology in parietal cortex of 5XFAD mice. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.
Belgrade: University of Belgrade, Faculty of Biology., 45.
https://hdl.handle.net/21.15107/rcub_ibiss_5804

Jović M, Lončarević-Vasiljković N, Avramović V, Brkić M, Milanović D, Kanazir S. Fish oil supplementation suppress neuritic dystrophy and Аβ pathology in parietal cortex of 5XFAD mice. in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia.. 2017;:45.
https://hdl.handle.net/21.15107/rcub_ibiss_5804 .

Jović, Milena, Lončarević-Vasiljković, Nataša, Avramović, Vladimir, Brkić, Marjana, Milanović, Desanka, Kanazir, Selma, "Fish oil supplementation suppress neuritic dystrophy and Аβ pathology in parietal cortex of 5XFAD mice" in Book of Abstracts: 1st Congress of Molecular Biologists of Serbia: CoMBoS; 2017 Sep 20-21; Belgrade, Serbia. (2017):45,
https://hdl.handle.net/21.15107/rcub_ibiss_5804 .

TY  - CONF
AU  - Lončarević-Vasiljković, Nataša
AU  - Jović, Milena
AU  - Ivković, Sanja
AU  - Milanović, Desanka
AU  - Brkić, Marjana
AU  - Avramović, Vladimir
AU  - Kanazir, Selma
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5715
AB  - Dystrophic neurites (DNs) are one of the neuropathological characteristics of Alzheimer's disease (AD) and represent the initial phase of neurodegeneration. Microtubule disruption in presynaptic dystrophic neurites that surround plaques impairs axonal transport and leads to the exacerbation of amyloid pathology in AD. Microglia plays a pivotal role in AD pathology as it is able to constitute a physical barrier around amyoid plaques and limit the accumulation of protofibrilar amylod beta around the fibrillar plaque core. In such a way microglia can mechanically shield the surrounding neurites from the neurotoxic protofibrillar Ai' aggregates. The use of supplements with omega-3 ( I%03) fatty acids (FAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), such as fish oil, is widespread due to proposed beneficial effects on the nervous system, High DHA consumption has been also associated with reduced risk and lessened AD pathology, yet the mechanisms and therapeutic potential of these supplements remain elusive. We analyzed the effects of the short-term fish oil (FO) supplementation on 4 months old 5xFAD mice, a mouse model with fast and robust development of the AD pathology hallmarks such as amyloid plaques and dystrophic neurites. We showed that even the short treatment with FO can affect the microglia clustering around amyloid plaques and increase the microglial plaque envelopment. Consequently, the Al2 accumulation was reduced and the appearance of DNs substantially suppressed. Our findings suggest that increased DHA consumption may play and important role in modulating microglial response and ameliorating AD pathology at least in the early phase of the disease.
PB  - Alzheimer's Association
C3  - AAIC Satellite Symposium: Aging and Alzheimer’s Disease: Opportunities for Therapeutic Interventions; 2017 Oct 19; Varna, Bulgaria
T1  - Short-term fish oil treatment suppresses the development of dystrophic neurites in the parietal cortex of 5XFAD AD mouse model during the early phase of the disease
SP  - 4B
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5715
ER  - 

@conference{
author = "Lončarević-Vasiljković, Nataša and Jović, Milena and Ivković, Sanja and Milanović, Desanka and Brkić, Marjana and Avramović, Vladimir and Kanazir, Selma",
year = "2017",
abstract = "Dystrophic neurites (DNs) are one of the neuropathological characteristics of Alzheimer's disease (AD) and represent the initial phase of neurodegeneration. Microtubule disruption in presynaptic dystrophic neurites that surround plaques impairs axonal transport and leads to the exacerbation of amyloid pathology in AD. Microglia plays a pivotal role in AD pathology as it is able to constitute a physical barrier around amyoid plaques and limit the accumulation of protofibrilar amylod beta around the fibrillar plaque core. In such a way microglia can mechanically shield the surrounding neurites from the neurotoxic protofibrillar Ai' aggregates. The use of supplements with omega-3 ( I%03) fatty acids (FAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), such as fish oil, is widespread due to proposed beneficial effects on the nervous system, High DHA consumption has been also associated with reduced risk and lessened AD pathology, yet the mechanisms and therapeutic potential of these supplements remain elusive. We analyzed the effects of the short-term fish oil (FO) supplementation on 4 months old 5xFAD mice, a mouse model with fast and robust development of the AD pathology hallmarks such as amyloid plaques and dystrophic neurites. We showed that even the short treatment with FO can affect the microglia clustering around amyloid plaques and increase the microglial plaque envelopment. Consequently, the Al2 accumulation was reduced and the appearance of DNs substantially suppressed. Our findings suggest that increased DHA consumption may play and important role in modulating microglial response and ameliorating AD pathology at least in the early phase of the disease.",
publisher = "Alzheimer's Association",
journal = "AAIC Satellite Symposium: Aging and Alzheimer’s Disease: Opportunities for Therapeutic Interventions; 2017 Oct 19; Varna, Bulgaria",
title = "Short-term fish oil treatment suppresses the development of dystrophic neurites in the parietal cortex of 5XFAD AD mouse model during the early phase of the disease",
pages = "4B",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5715"
}

Lončarević-Vasiljković, N., Jović, M., Ivković, S., Milanović, D., Brkić, M., Avramović, V.,& Kanazir, S.. (2017). Short-term fish oil treatment suppresses the development of dystrophic neurites in the parietal cortex of 5XFAD AD mouse model during the early phase of the disease. in AAIC Satellite Symposium: Aging and Alzheimer’s Disease: Opportunities for Therapeutic Interventions; 2017 Oct 19; Varna, Bulgaria
Alzheimer's Association., 4B.
https://hdl.handle.net/21.15107/rcub_ibiss_5715

Lončarević-Vasiljković N, Jović M, Ivković S, Milanović D, Brkić M, Avramović V, Kanazir S. Short-term fish oil treatment suppresses the development of dystrophic neurites in the parietal cortex of 5XFAD AD mouse model during the early phase of the disease. in AAIC Satellite Symposium: Aging and Alzheimer’s Disease: Opportunities for Therapeutic Interventions; 2017 Oct 19; Varna, Bulgaria. 2017;:4B.
https://hdl.handle.net/21.15107/rcub_ibiss_5715 .

Lončarević-Vasiljković, Nataša, Jović, Milena, Ivković, Sanja, Milanović, Desanka, Brkić, Marjana, Avramović, Vladimir, Kanazir, Selma, "Short-term fish oil treatment suppresses the development of dystrophic neurites in the parietal cortex of 5XFAD AD mouse model during the early phase of the disease" in AAIC Satellite Symposium: Aging and Alzheimer’s Disease: Opportunities for Therapeutic Interventions; 2017 Oct 19; Varna, Bulgaria (2017):4B,
https://hdl.handle.net/21.15107/rcub_ibiss_5715 .

TY  - CONF
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Milanović, Desanka
AU  - Avramović, Vladimir
AU  - Brkić, Marjana
AU  - Kanazir, Selma
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5714
AB  - Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory loss and dementia. Pathologically, the disease is recognized by the presence of senile plaques (deposition of beta amyloid (Ap) peptides), neurofibrillary tangles, and neuronal loss. Clustering of microglial cells at sites of AO deposition in the brain is also an important pathological feature of AD. At present, there is no effective treatment for AD. 
To investigate the influence of fish oil (FO) supplementation, like potential treatment, we used transgenic 5xFAD mice which rapidly recapitulate major hallmarks of AD amyloid pathology. Three-month old female 5xFAD mice received FO (1001d/animallday) via oral gavage during 3 weeks period. Histological analysis was used to detect changes in pathological features of AD in parietal cortex in 5xFAD mice.ThioflavinS and AmiloGlo were used to visualize plaques, soluble Ap peptide was detect by A1342 antibody, SM131 antibody was used for neuritic dystrophy and lba-1 antibody for microglial cells. lmmunostaining was observed by confocal microscopy. Quantification was done by Image J program. 
We showed that short-term FO supplementation is capable of inducing significant decreased of number of plaques, total All levels, and preventing the emergence of neuritic dystrophy in parietal cortex of 5xFAD mice. Also, FO supplementation led to increase in overall microglial number, and enhanced clustering of microglial cells around amyloid plaques. We confirmed and extended previous findings suggesting that FO has a typical pleiotropic effect and we believe that FO in combination with others drugs could be good approach for long-term treatment in AD suppression.
PB  - Belgrade: Institute of Physics
C3  - Book of Abstracts: the Sixth International School and Conference on Photonics & COST actions: MP1406 and MP1402 & H2020-MSCA-RISE-2015 CARDIALLY workshop: PHOTONICA2017; 2017 Aug 28 - Sep 1; Belgrade, Serbia
T1  - The effect of short-term fish oil supplementation on Alzheimer disease-like pathology in 5xFAD mouse model
SP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5714
ER  - 

@conference{
author = "Jović, Milena and Lončarević-Vasiljković, Nataša and Milanović, Desanka and Avramović, Vladimir and Brkić, Marjana and Kanazir, Selma",
year = "2017",
abstract = "Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory loss and dementia. Pathologically, the disease is recognized by the presence of senile plaques (deposition of beta amyloid (Ap) peptides), neurofibrillary tangles, and neuronal loss. Clustering of microglial cells at sites of AO deposition in the brain is also an important pathological feature of AD. At present, there is no effective treatment for AD. 
To investigate the influence of fish oil (FO) supplementation, like potential treatment, we used transgenic 5xFAD mice which rapidly recapitulate major hallmarks of AD amyloid pathology. Three-month old female 5xFAD mice received FO (1001d/animallday) via oral gavage during 3 weeks period. Histological analysis was used to detect changes in pathological features of AD in parietal cortex in 5xFAD mice.ThioflavinS and AmiloGlo were used to visualize plaques, soluble Ap peptide was detect by A1342 antibody, SM131 antibody was used for neuritic dystrophy and lba-1 antibody for microglial cells. lmmunostaining was observed by confocal microscopy. Quantification was done by Image J program. 
We showed that short-term FO supplementation is capable of inducing significant decreased of number of plaques, total All levels, and preventing the emergence of neuritic dystrophy in parietal cortex of 5xFAD mice. Also, FO supplementation led to increase in overall microglial number, and enhanced clustering of microglial cells around amyloid plaques. We confirmed and extended previous findings suggesting that FO has a typical pleiotropic effect and we believe that FO in combination with others drugs could be good approach for long-term treatment in AD suppression.",
publisher = "Belgrade: Institute of Physics",
journal = "Book of Abstracts: the Sixth International School and Conference on Photonics & COST actions: MP1406 and MP1402 & H2020-MSCA-RISE-2015 CARDIALLY workshop: PHOTONICA2017; 2017 Aug 28 - Sep 1; Belgrade, Serbia",
title = "The effect of short-term fish oil supplementation on Alzheimer disease-like pathology in 5xFAD mouse model",
pages = "126",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5714"
}

Jović, M., Lončarević-Vasiljković, N., Milanović, D., Avramović, V., Brkić, M.,& Kanazir, S.. (2017). The effect of short-term fish oil supplementation on Alzheimer disease-like pathology in 5xFAD mouse model. in Book of Abstracts: the Sixth International School and Conference on Photonics & COST actions: MP1406 and MP1402 & H2020-MSCA-RISE-2015 CARDIALLY workshop: PHOTONICA2017; 2017 Aug 28 - Sep 1; Belgrade, Serbia
Belgrade: Institute of Physics., 126.
https://hdl.handle.net/21.15107/rcub_ibiss_5714

Jović M, Lončarević-Vasiljković N, Milanović D, Avramović V, Brkić M, Kanazir S. The effect of short-term fish oil supplementation on Alzheimer disease-like pathology in 5xFAD mouse model. in Book of Abstracts: the Sixth International School and Conference on Photonics & COST actions: MP1406 and MP1402 & H2020-MSCA-RISE-2015 CARDIALLY workshop: PHOTONICA2017; 2017 Aug 28 - Sep 1; Belgrade, Serbia. 2017;:126.
https://hdl.handle.net/21.15107/rcub_ibiss_5714 .

Jović, Milena, Lončarević-Vasiljković, Nataša, Milanović, Desanka, Avramović, Vladimir, Brkić, Marjana, Kanazir, Selma, "The effect of short-term fish oil supplementation on Alzheimer disease-like pathology in 5xFAD mouse model" in Book of Abstracts: the Sixth International School and Conference on Photonics & COST actions: MP1406 and MP1402 & H2020-MSCA-RISE-2015 CARDIALLY workshop: PHOTONICA2017; 2017 Aug 28 - Sep 1; Belgrade, Serbia (2017):126,
https://hdl.handle.net/21.15107/rcub_ibiss_5714 .

TY  - JOUR
AU  - Milanović, Desanka
AU  - Pešić, Vesna
AU  - Lončarević-Vasiljković, Nataša
AU  - Pavković, Željko
AU  - Popić, Jelena
AU  - Kanazir, Selma
AU  - Jevtović-Todorović, Vesna
AU  - Ruždijić, Sabera
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5457
AB  - A number of experimental studies have reported that exposure to common, clinically used anesthetics induce extensive neuroapoptosis and cognitive impairment when applied to young rodents, up to 2 weeks old, in phase of rapid synaptogenesis. Propofol is the most used general anesthetic in clinical practice whose mechanisms of neurotoxicity on the developing brain remains to be examined in depth. This study investigated effects of different exposures to propofol anesthesia on Fas receptor and Fas ligand expressions, which mediate proapoptotic and proinflammation signaling in the brain. Propofol (20 mg/kg) was administered to 7-day-old rats in multiple doses sufficient to maintain 2-, 4- and 6-h duration of anesthesia. Animals were sacrificed at 0, 4, 16 and 24 h after termination of anesthesia. It was found that propofol anesthesia induced Fas/FasL and downstream caspase-8 expression more prominently in the thalamus than in the cortex. Opposite, Bcl-2 and caspase-9, markers of intrinsic pathway activation, were shown to be more influenced by propofol treatment in the cortex. Further, we have established upregulation of caspase-1 and IL-1β cytokine transcription as well as subsequent activation of microglia that is potentially associated with brain inflammation. Behavioral analyses revealed that P35 and P60 animals, neonatally exposed to propofol, had significantly higher motor activity during three consecutive days of testing in the open field, though formation of the intersession habituation was not prevented. This data, together with our previous results, contributes to elucidation of complex mechanisms of propofol toxicity in developing brain.
PB  - New York: Springer
T2  - Neurotoxicity Research
T1  - The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats
IS  - 3
VL  - 30
DO  - 10.1007/s12640-016-9629-1
SP  - 434
EP  - 452
ER  - 

@article{
author = "Milanović, Desanka and Pešić, Vesna and Lončarević-Vasiljković, Nataša and Pavković, Željko and Popić, Jelena and Kanazir, Selma and Jevtović-Todorović, Vesna and Ruždijić, Sabera",
year = "2016",
abstract = "A number of experimental studies have reported that exposure to common, clinically used anesthetics induce extensive neuroapoptosis and cognitive impairment when applied to young rodents, up to 2 weeks old, in phase of rapid synaptogenesis. Propofol is the most used general anesthetic in clinical practice whose mechanisms of neurotoxicity on the developing brain remains to be examined in depth. This study investigated effects of different exposures to propofol anesthesia on Fas receptor and Fas ligand expressions, which mediate proapoptotic and proinflammation signaling in the brain. Propofol (20 mg/kg) was administered to 7-day-old rats in multiple doses sufficient to maintain 2-, 4- and 6-h duration of anesthesia. Animals were sacrificed at 0, 4, 16 and 24 h after termination of anesthesia. It was found that propofol anesthesia induced Fas/FasL and downstream caspase-8 expression more prominently in the thalamus than in the cortex. Opposite, Bcl-2 and caspase-9, markers of intrinsic pathway activation, were shown to be more influenced by propofol treatment in the cortex. Further, we have established upregulation of caspase-1 and IL-1β cytokine transcription as well as subsequent activation of microglia that is potentially associated with brain inflammation. Behavioral analyses revealed that P35 and P60 animals, neonatally exposed to propofol, had significantly higher motor activity during three consecutive days of testing in the open field, though formation of the intersession habituation was not prevented. This data, together with our previous results, contributes to elucidation of complex mechanisms of propofol toxicity in developing brain.",
publisher = "New York: Springer",
journal = "Neurotoxicity Research",
title = "The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats",
number = "3",
volume = "30",
doi = "10.1007/s12640-016-9629-1",
pages = "434-452"
}

Milanović, D., Pešić, V., Lončarević-Vasiljković, N., Pavković, Ž., Popić, J., Kanazir, S., Jevtović-Todorović, V.,& Ruždijić, S.. (2016). The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats. in Neurotoxicity Research
New York: Springer., 30(3), 434-452.
https://doi.org/10.1007/s12640-016-9629-1

Milanović D, Pešić V, Lončarević-Vasiljković N, Pavković Ž, Popić J, Kanazir S, Jevtović-Todorović V, Ruždijić S. The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats. in Neurotoxicity Research. 2016;30(3):434-452.
doi:10.1007/s12640-016-9629-1 .

Milanović, Desanka, Pešić, Vesna, Lončarević-Vasiljković, Nataša, Pavković, Željko, Popić, Jelena, Kanazir, Selma, Jevtović-Todorović, Vesna, Ruždijić, Sabera, "The Fas Ligand/Fas Death Receptor Pathways Contribute to Propofol-Induced Apoptosis and Neuroinflammation in the Brain of Neonatal Rats" in Neurotoxicity Research, 30, no. 3 (2016):434-452,
https://doi.org/10.1007/s12640-016-9629-1 . .

TY  - JOUR
AU  - Lončarević-Vasiljković, Nataša
AU  - Milanović, Desanka
AU  - Pešić, Vesna
AU  - Tešić, Vesna
AU  - Brkić, Marjana
AU  - Lazić, Divna
AU  - Avramović, Vladimir
AU  - Kanazir, Selma
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5437
AB  - Subsequent pathological events occurring in the brain after TBI, referred to as secondary injury, continue to damage surrounding tissue resulting in substantial neuronal loss. Using an animal model of TBI we examined the effect of dietary restriction (DR) on the neuroapoptosis and Bcl-2 family genes as the main regulators of the intrinsic apoptotic pathway. Bcl-2, Bcl-xl and Bax mRNA and protein expression in the ipsilateral cortex of adult Wistar rats exposed to DR before TBI were studied from 2 to 28 days post injury. Our results showed that DR suppressed neuroapoptosis and promoted significant upregulation of antiapoptotic Bcl-2 and Bcl-xl mRNAs in the ipsilateral cortex following injury. Expression of the proapoptotic Bax gene increased in ad libitum (AL) fed rats but remained unchanged in rats exposed to DR. Although the expression of Bcl-2, Bcl-xl and Bax proteins was changed in a similar manner in both experimental groups, DR promoted a continuous increase in the Bcl-2:Bax protein ratio throughout the recovery period. Together with our previous finding that DR mediates inhibition of the extrinsic apoptotic pathway the present work reveals that modulation of the intrinsic pathway contributes to the beneficial effect of DR in brain injury. These findings provide new insight into the effects of DR on pro-survival signaling after injury, lending further support to its neuroprotective effect.
PB  - England : Elsevier
T2  - Neurochemistry International
T1  - Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury.
VL  - 96
DO  - 10.1016/j.neuint.2016.02.017
SP  - 69
EP  - 76
ER  - 

@article{
author = "Lončarević-Vasiljković, Nataša and Milanović, Desanka and Pešić, Vesna and Tešić, Vesna and Brkić, Marjana and Lazić, Divna and Avramović, Vladimir and Kanazir, Selma",
year = "2016",
abstract = "Subsequent pathological events occurring in the brain after TBI, referred to as secondary injury, continue to damage surrounding tissue resulting in substantial neuronal loss. Using an animal model of TBI we examined the effect of dietary restriction (DR) on the neuroapoptosis and Bcl-2 family genes as the main regulators of the intrinsic apoptotic pathway. Bcl-2, Bcl-xl and Bax mRNA and protein expression in the ipsilateral cortex of adult Wistar rats exposed to DR before TBI were studied from 2 to 28 days post injury. Our results showed that DR suppressed neuroapoptosis and promoted significant upregulation of antiapoptotic Bcl-2 and Bcl-xl mRNAs in the ipsilateral cortex following injury. Expression of the proapoptotic Bax gene increased in ad libitum (AL) fed rats but remained unchanged in rats exposed to DR. Although the expression of Bcl-2, Bcl-xl and Bax proteins was changed in a similar manner in both experimental groups, DR promoted a continuous increase in the Bcl-2:Bax protein ratio throughout the recovery period. Together with our previous finding that DR mediates inhibition of the extrinsic apoptotic pathway the present work reveals that modulation of the intrinsic pathway contributes to the beneficial effect of DR in brain injury. These findings provide new insight into the effects of DR on pro-survival signaling after injury, lending further support to its neuroprotective effect.",
publisher = "England : Elsevier",
journal = "Neurochemistry International",
title = "Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury.",
volume = "96",
doi = "10.1016/j.neuint.2016.02.017",
pages = "69-76"
}

Lončarević-Vasiljković, N., Milanović, D., Pešić, V., Tešić, V., Brkić, M., Lazić, D., Avramović, V.,& Kanazir, S.. (2016). Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury.. in Neurochemistry International
England : Elsevier., 96, 69-76.
https://doi.org/10.1016/j.neuint.2016.02.017

Lončarević-Vasiljković N, Milanović D, Pešić V, Tešić V, Brkić M, Lazić D, Avramović V, Kanazir S. Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury.. in Neurochemistry International. 2016;96:69-76.
doi:10.1016/j.neuint.2016.02.017 .

Lončarević-Vasiljković, Nataša, Milanović, Desanka, Pešić, Vesna, Tešić, Vesna, Brkić, Marjana, Lazić, Divna, Avramović, Vladimir, Kanazir, Selma, "Dietary restriction suppresses apoptotic cell death, promotes Bcl-2 and Bcl-xl mRNA expression and increases the Bcl-2/Bax protein ratio in the rat cortex after cortical injury." in Neurochemistry International, 96 (2016):69-76,
https://doi.org/10.1016/j.neuint.2016.02.017 . .

TY  - JOUR
AU  - Lončarević-Vasiljković, Nataša
AU  - Pešić, Vesna
AU  - Tanić, N.
AU  - Milanović, Desanka
AU  - Mladenović, Aleksandra
AU  - Perović, Milka
AU  - Kanazir, Selma
AU  - Ruždijić, Sabera
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/328
AB  - The recovery period following cortical injury (CI) is characterized by a dynamic and highly complex interplay between beneficial and detrimental events. The aim of this study was to examine the expressions of Glial Fibrillary Acidic Protein (GFAP), Apolipoprotein E (ApoE) and Amyloid Precursor Protein (APP), all of which are involved in brain plasticity and neurodegeneration. Our results reveal that CI strongly influenced GFAP, ApoE and APP mRNA expression, as well as GFAP and ApoE protein expression. Considering the pivotal role of these proteins in the brain, the obtained results point to their potential contribution in neurodegeneration and consequent Alzheimer's disease development.
T2  - Archives of Biological Sciences
T1  - Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury
IS  - 1
VL  - 65
SP  - 255
EP  - 264
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_328
ER  - 

@article{
author = "Lončarević-Vasiljković, Nataša and Pešić, Vesna and Tanić, N. and Milanović, Desanka and Mladenović, Aleksandra and Perović, Milka and Kanazir, Selma and Ruždijić, Sabera",
year = "2013, 2013",
abstract = "The recovery period following cortical injury (CI) is characterized by a dynamic and highly complex interplay between beneficial and detrimental events. The aim of this study was to examine the expressions of Glial Fibrillary Acidic Protein (GFAP), Apolipoprotein E (ApoE) and Amyloid Precursor Protein (APP), all of which are involved in brain plasticity and neurodegeneration. Our results reveal that CI strongly influenced GFAP, ApoE and APP mRNA expression, as well as GFAP and ApoE protein expression. Considering the pivotal role of these proteins in the brain, the obtained results point to their potential contribution in neurodegeneration and consequent Alzheimer's disease development.",
journal = "Archives of Biological Sciences",
title = "Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury",
number = "1",
volume = "65",
pages = "255-264",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_328"
}

Lončarević-Vasiljković, N., Pešić, V., Tanić, N., Milanović, D., Mladenović, A., Perović, M., Kanazir, S.,& Ruždijić, S.. (2013). Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury. in Archives of Biological Sciences, 65(1), 255-264.
https://hdl.handle.net/21.15107/rcub_ibiss_328

Lončarević-Vasiljković N, Pešić V, Tanić N, Milanović D, Mladenović A, Perović M, Kanazir S, Ruždijić S. Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury. in Archives of Biological Sciences. 2013;65(1):255-264.
https://hdl.handle.net/21.15107/rcub_ibiss_328 .

Lončarević-Vasiljković, Nataša, Pešić, Vesna, Tanić, N., Milanović, Desanka, Mladenović, Aleksandra, Perović, Milka, Kanazir, Selma, Ruždijić, Sabera, "Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury" in Archives of Biological Sciences, 65, no. 1 (2013):255-264,
https://hdl.handle.net/21.15107/rcub_ibiss_328 .

TY  - JOUR
AU  - Perović, Milka
AU  - Tesić, Vesna T
AU  - Mladenović, Aleksandra
AU  - Smiljanić, Kosara
AU  - Lončarević-Vasiljković, Nataša
AU  - Ruždijić, Sabera
AU  - Kanazir, Selma
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/946
AB  - Neurotrophins are established molecular mediators of neuronal plasticity in the adult brain. We analyzed the impact of aging on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) protein isoforms, their receptors, and on the expression patterns of multiple 5' exon-specific BDNF transcripts in the rat cortex and hippocampus throughout the life span of the rat (6, 12, 18, and 24 months of age). ProNGF was increased during aging in both structures. Mature NGF gradually decreased in the cortex, and, in 24-month-old animals, it was 30 % lower than that in adult 6-month-old rats. The BDNF expression did not change during aging, while proBDNF accumulated in the hippocampus of aged rats. Hippocampal total BDNF mRNA was lower in 12-month-old animals, mostly as a result of a decrease of BDNF transcripts 1 and 2. In contrast to the region-specific regulation of specific exon-containing BDNF mRNAs in adult animals, the same BDNF RNA isoforms (containing exons III, IV, or VI) were present in both brain structures of aged animals. Deficits in neurotrophin signaling were supported by the observed decrease in Trk receptor expression which was accompanied by lower levels of the two main downstream effector kinases, pAkt and protein kinase C. The proteolytic processing of p75NTR observed in 12-month-old rats points to an additional regulatory mechanism in early aging. The changes described herein could contribute to reduced brain plasticity underlying the age-dependent decline in cognitive function.
T2  - Age
T1  - BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat
IS  - 6
VL  - 35
SP  - 233
EP  - 2070
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_946
ER  - 

@article{
author = "Perović, Milka and Tesić, Vesna T and Mladenović, Aleksandra and Smiljanić, Kosara and Lončarević-Vasiljković, Nataša and Ruždijić, Sabera and Kanazir, Selma",
year = "2013",
abstract = "Neurotrophins are established molecular mediators of neuronal plasticity in the adult brain. We analyzed the impact of aging on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) protein isoforms, their receptors, and on the expression patterns of multiple 5' exon-specific BDNF transcripts in the rat cortex and hippocampus throughout the life span of the rat (6, 12, 18, and 24 months of age). ProNGF was increased during aging in both structures. Mature NGF gradually decreased in the cortex, and, in 24-month-old animals, it was 30 % lower than that in adult 6-month-old rats. The BDNF expression did not change during aging, while proBDNF accumulated in the hippocampus of aged rats. Hippocampal total BDNF mRNA was lower in 12-month-old animals, mostly as a result of a decrease of BDNF transcripts 1 and 2. In contrast to the region-specific regulation of specific exon-containing BDNF mRNAs in adult animals, the same BDNF RNA isoforms (containing exons III, IV, or VI) were present in both brain structures of aged animals. Deficits in neurotrophin signaling were supported by the observed decrease in Trk receptor expression which was accompanied by lower levels of the two main downstream effector kinases, pAkt and protein kinase C. The proteolytic processing of p75NTR observed in 12-month-old rats points to an additional regulatory mechanism in early aging. The changes described herein could contribute to reduced brain plasticity underlying the age-dependent decline in cognitive function.",
journal = "Age",
title = "BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat",
number = "6",
volume = "35",
pages = "233-2070",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_946"
}

Perović, M., Tesić, V. T., Mladenović, A., Smiljanić, K., Lončarević-Vasiljković, N., Ruždijić, S.,& Kanazir, S.. (2013). BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat. in Age, 35(6), 233-2070.
https://hdl.handle.net/21.15107/rcub_ibiss_946

Perović M, Tesić VT, Mladenović A, Smiljanić K, Lončarević-Vasiljković N, Ruždijić S, Kanazir S. BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat. in Age. 2013;35(6):233-2070.
https://hdl.handle.net/21.15107/rcub_ibiss_946 .

Perović, Milka, Tesić, Vesna T, Mladenović, Aleksandra, Smiljanić, Kosara, Lončarević-Vasiljković, Nataša, Ruždijić, Sabera, Kanazir, Selma, "BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat" in Age, 35, no. 6 (2013):233-2070,
https://hdl.handle.net/21.15107/rcub_ibiss_946 .

TY  - CONF
AU  - Lazić, D
AU  - Tesić, V
AU  - Brkić, Marjana P.
AU  - Lončarević-Vasiljković, Nataša
AU  - Perović, Milka
AU  - Mladenović, Aleksandra
AU  - Rakić, Lj
AU  - Kanazir, Selma
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/976
C3  - Free Radical Biology and Medicine
T1  - Influence of dietary restriction on astrocytic response in the rat brain following traumatic brain injury
IS  - null
VL  - 65
SP  - 607
EP  - S17
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_976
ER  - 

@conference{
author = "Lazić, D and Tesić, V and Brkić, Marjana P. and Lončarević-Vasiljković, Nataša and Perović, Milka and Mladenović, Aleksandra and Rakić, Lj and Kanazir, Selma",
year = "2013",
journal = "Free Radical Biology and Medicine",
title = "Influence of dietary restriction on astrocytic response in the rat brain following traumatic brain injury",
number = "null",
volume = "65",
pages = "607-S17",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_976"
}

Lazić, D., Tesić, V., Brkić, M. P., Lončarević-Vasiljković, N., Perović, M., Mladenović, A., Rakić, L.,& Kanazir, S.. (2013). Influence of dietary restriction on astrocytic response in the rat brain following traumatic brain injury. in Free Radical Biology and Medicine, 65(null), 607-S17.
https://hdl.handle.net/21.15107/rcub_ibiss_976

Lazić D, Tesić V, Brkić MP, Lončarević-Vasiljković N, Perović M, Mladenović A, Rakić L, Kanazir S. Influence of dietary restriction on astrocytic response in the rat brain following traumatic brain injury. in Free Radical Biology and Medicine. 2013;65(null):607-S17.
https://hdl.handle.net/21.15107/rcub_ibiss_976 .

Lazić, D, Tesić, V, Brkić, Marjana P., Lončarević-Vasiljković, Nataša, Perović, Milka, Mladenović, Aleksandra, Rakić, Lj, Kanazir, Selma, "Influence of dietary restriction on astrocytic response in the rat brain following traumatic brain injury" in Free Radical Biology and Medicine, 65, no. null (2013):607-S17,
https://hdl.handle.net/21.15107/rcub_ibiss_976 .