TY  - CONF
AU  - Jovanović Macura, Irena
AU  - Đuričić, Ivana
AU  - Major, Tamara
AU  - Milanović, Desanka
AU  - Brkić, Marjana
AU  - Sobajić, Slađana
AU  - Kanazir, Selma
AU  - Ivković, Sanja
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5858
AB  - Mfsd2a is expressed mainly in the endothelial cells and is an essential regulator of 
blood vessel transcytosis. Therefore, decrease in Mfsd2a expression can be a risk 
factor for developing leaky blood vessels. Mfsd2a is also the main docosahexaenoic 
acid (DHA, C22:6n3) transporter. DHA, an omega-3 fatty acid, is one of the main 
structural lipids of the neuronal and vascular retina, crucial for the normal functioning 
of photoreceptors (PRs). However, the capacity of the retina to synthesize DHA is 
limited, and the maintenance of retinal DHA content relies on the uptake from blood borne lipids. The currently recommended FO doses yielded low PUFAs tissue 
bioavailability, and supplementation with higher doses has been increasingly 
recommended. Nevertheless, the effects of higher FO doses on retinal Mfsd2a 
expression and blood vessels coverage are unknown.
Western blot and qPCR analyses showed that high dose FO supplementation increased 
Mfsd2a expression in the retina. Immunohistochemical analyses of Mfsd2a expression 
on retinal blood vessels (labeled with 488-conjugated Lycopersicon esculentum, 
lectin) and subsequent ImageJ analyses revealed 1.32-fold increase in the Mfsd2a 
retinal blood vessel coverage. In the same time the pericyte blood vessel coverage 
(CD13+ cells) was not affected with FO supplementation, and the increase in Mfsd2a 
blood vessel expression is not the result of the increased pericyte coverage. 
Therefore, the high-dose FO supplementation emerges as the prophylactic fortifier of 
the retinal blood vessels that can serve either as prophylaxis in the healthy eye or as an 
adjuvant in developing targeted manipulations of the barrier during diseases.
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  - The high-dose fish oil (FO) supplementation increased Mfsd2a expression in the retina of healthy mice
SP  - 66
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5858
ER  - 

@conference{
author = "Jovanović Macura, Irena and Đuričić, Ivana and Major, Tamara and Milanović, Desanka and Brkić, Marjana and Sobajić, Slađana and Kanazir, Selma and Ivković, Sanja",
year = "2023",
abstract = "Mfsd2a is expressed mainly in the endothelial cells and is an essential regulator of 
blood vessel transcytosis. Therefore, decrease in Mfsd2a expression can be a risk 
factor for developing leaky blood vessels. Mfsd2a is also the main docosahexaenoic 
acid (DHA, C22:6n3) transporter. DHA, an omega-3 fatty acid, is one of the main 
structural lipids of the neuronal and vascular retina, crucial for the normal functioning 
of photoreceptors (PRs). However, the capacity of the retina to synthesize DHA is 
limited, and the maintenance of retinal DHA content relies on the uptake from blood borne lipids. The currently recommended FO doses yielded low PUFAs tissue 
bioavailability, and supplementation with higher doses has been increasingly 
recommended. Nevertheless, the effects of higher FO doses on retinal Mfsd2a 
expression and blood vessels coverage are unknown.
Western blot and qPCR analyses showed that high dose FO supplementation increased 
Mfsd2a expression in the retina. Immunohistochemical analyses of Mfsd2a expression 
on retinal blood vessels (labeled with 488-conjugated Lycopersicon esculentum, 
lectin) and subsequent ImageJ analyses revealed 1.32-fold increase in the Mfsd2a 
retinal blood vessel coverage. In the same time the pericyte blood vessel coverage 
(CD13+ cells) was not affected with FO supplementation, and the increase in Mfsd2a 
blood vessel expression is not the result of the increased pericyte coverage. 
Therefore, the high-dose FO supplementation emerges as the prophylactic fortifier of 
the retinal blood vessels that can serve either as prophylaxis in the healthy eye or as an 
adjuvant in developing targeted manipulations of the barrier during diseases.",
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 = "The high-dose fish oil (FO) supplementation increased Mfsd2a expression in the retina of healthy mice",
pages = "66",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5858"
}

Jovanović Macura, I., Đuričić, I., Major, T., Milanović, D., Brkić, M., Sobajić, S., Kanazir, S.,& Ivković, S.. (2023). The high-dose fish oil (FO) supplementation increased Mfsd2a expression in the retina of healthy 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., 66.
https://hdl.handle.net/21.15107/rcub_ibiss_5858

Jovanović Macura I, Đuričić I, Major T, Milanović D, Brkić M, Sobajić S, Kanazir S, Ivković S. The high-dose fish oil (FO) supplementation increased Mfsd2a expression in the retina of healthy mice. in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia. 2023;:66.
https://hdl.handle.net/21.15107/rcub_ibiss_5858 .

Jovanović Macura, Irena, Đuričić, Ivana, Major, Tamara, Milanović, Desanka, Brkić, Marjana, Sobajić, Slađana, Kanazir, Selma, Ivković, Sanja, "The high-dose fish oil (FO) supplementation increased Mfsd2a expression in the retina of healthy mice" in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia (2023):66,
https://hdl.handle.net/21.15107/rcub_ibiss_5858 .

TY  - JOUR
AU  - Jovanović Macura, Irena
AU  - Đuričić, Ivana
AU  - Major, Tamara
AU  - Milanović, Desanka
AU  - Brkić, Marjana
AU  - Šobajić, Slađana
AU  - Kanazir, Selma
AU  - Ivković, Sanja
PY  - 2022
UR  - https://linkinghub.elsevier.com/retrieve/pii/S1756464622003723
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5174
AB  - The recommended fish oil (FO) supplementation doses often yield low omega-3 polyunsaturated fatty acids (PUFAs) tissue bioavailability, and higher doses (up to 10 g per day) have been increasingly recommended. However, the exact effects of such FO supplementation on the healthy retina and retinal pigmented epithelium (RPE) are unknown. Our study showed that the high dose FO treatment did not imbalance the rigorous docosahexaenoic acid (DHA, C22:6n3) homeostasis in the retina and RPE in the three-month-old female B6/SLJ mice. Instead, we have found the significant increase in the expression of Mfsd2a, the main DHA transporter. Mfsd2a is also an essential regulator of blood vessel transcytosis and the decrease in Mfsd2a expression can be a risk factor for developing leaky blood vessels. Therefore, the high-dose FO supplementation emerges as the prophylactic fortifier of the retinal blood vessels.
T2  - Journal of Functional Foods
T1  - The high-dose fish oil supplementation increased Mfsd2a expression without altering DHA levels in the retina of healthy mice
VL  - 99
DO  - 10.1016/j.jff.2022.105302
SP  - 105302
ER  - 

@article{
author = "Jovanović Macura, Irena and Đuričić, Ivana and Major, Tamara and Milanović, Desanka and Brkić, Marjana and Šobajić, Slađana and Kanazir, Selma and Ivković, Sanja",
year = "2022",
abstract = "The recommended fish oil (FO) supplementation doses often yield low omega-3 polyunsaturated fatty acids (PUFAs) tissue bioavailability, and higher doses (up to 10 g per day) have been increasingly recommended. However, the exact effects of such FO supplementation on the healthy retina and retinal pigmented epithelium (RPE) are unknown. Our study showed that the high dose FO treatment did not imbalance the rigorous docosahexaenoic acid (DHA, C22:6n3) homeostasis in the retina and RPE in the three-month-old female B6/SLJ mice. Instead, we have found the significant increase in the expression of Mfsd2a, the main DHA transporter. Mfsd2a is also an essential regulator of blood vessel transcytosis and the decrease in Mfsd2a expression can be a risk factor for developing leaky blood vessels. Therefore, the high-dose FO supplementation emerges as the prophylactic fortifier of the retinal blood vessels.",
journal = "Journal of Functional Foods",
title = "The high-dose fish oil supplementation increased Mfsd2a expression without altering DHA levels in the retina of healthy mice",
volume = "99",
doi = "10.1016/j.jff.2022.105302",
pages = "105302"
}

Jovanović Macura, I., Đuričić, I., Major, T., Milanović, D., Brkić, M., Šobajić, S., Kanazir, S.,& Ivković, S.. (2022). The high-dose fish oil supplementation increased Mfsd2a expression without altering DHA levels in the retina of healthy mice. in Journal of Functional Foods, 99, 105302.
https://doi.org/10.1016/j.jff.2022.105302

Jovanović Macura I, Đuričić I, Major T, Milanović D, Brkić M, Šobajić S, Kanazir S, Ivković S. The high-dose fish oil supplementation increased Mfsd2a expression without altering DHA levels in the retina of healthy mice. in Journal of Functional Foods. 2022;99:105302.
doi:10.1016/j.jff.2022.105302 .

Jovanović Macura, Irena, Đuričić, Ivana, Major, Tamara, Milanović, Desanka, Brkić, Marjana, Šobajić, Slađana, Kanazir, Selma, Ivković, Sanja, "The high-dose fish oil supplementation increased Mfsd2a expression without altering DHA levels in the retina of healthy mice" in Journal of Functional Foods, 99 (2022):105302,
https://doi.org/10.1016/j.jff.2022.105302 . .

TY  - JOUR
AU  - Vandendriessche, Charysse
AU  - Balusu, Sriram
AU  - Van Cauwenberghe, Caroline
AU  - Brkić, Marjana
AU  - Pauwels, Marie
AU  - Plehiers, Nele
AU  - Bruggeman, Arnout
AU  - Dujardin, Pieter
AU  - Van Imschoot, Griet
AU  - Van Wonterghem, Elien
AU  - Hendrix, An
AU  - Baeke, Femke
AU  - De Rycke, Riet
AU  - Gevaert, Kris
AU  - Vandenbroucke, Roosmarijn E.
PY  - 2021
UR  - https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-021-01245-z
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC8381545
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4476
AB  - Increasing evidence indicates that extracellular vesicles (EVs) play an important role in the pathogenesis of Alzheimer's disease (AD). We previously reported that the blood-cerebrospinal fluid (CSF) interface, formed by the choroid plexus epithelial (CPE) cells, releases an increased amount of EVs into the CSF in response to peripheral inflammation. Here, we studied the importance of CP-mediated EV release in AD pathogenesis. We observed increased EV levels in the CSF of young transgenic APP/PS1 mice which correlated with high amyloid beta (Aβ) CSF levels at this age. The intracerebroventricular (icv) injection of Aβ oligomers (AβO) in wild-type mice revealed a significant increase of EVs in the CSF, signifying that the presence of CSF-AβO is sufficient to induce increased EV secretion. Using in vivo, in vitro and ex vivo approaches, we identified the CP as a major source of the CSF-EVs. Interestingly, AβO-induced, CP-derived EVs induced pro-inflammatory effects in mixed cortical cultures. Proteome analysis of these EVs revealed the presence of several pro-inflammatory proteins, including the complement protein C3. Strikingly, inhibition of EV production using GW4869 resulted in protection against acute AβO-induced cognitive decline. Further research into the underlying mechanisms of this EV secretion might open up novel therapeutic strategies to impact the pathogenesis and progression of AD.
T2  - Acta Neuropathologica Communications
T1  - Importance of extracellular vesicle secretion at the blood-cerebrospinal fluid interface in the pathogenesis of Alzheimer's disease.
IS  - 1
VL  - 9
DO  - 10.1186/s40478-021-01245-z
SP  - 143
ER  - 

@article{
author = "Vandendriessche, Charysse and Balusu, Sriram and Van Cauwenberghe, Caroline and Brkić, Marjana and Pauwels, Marie and Plehiers, Nele and Bruggeman, Arnout and Dujardin, Pieter and Van Imschoot, Griet and Van Wonterghem, Elien and Hendrix, An and Baeke, Femke and De Rycke, Riet and Gevaert, Kris and Vandenbroucke, Roosmarijn E.",
year = "2021",
abstract = "Increasing evidence indicates that extracellular vesicles (EVs) play an important role in the pathogenesis of Alzheimer's disease (AD). We previously reported that the blood-cerebrospinal fluid (CSF) interface, formed by the choroid plexus epithelial (CPE) cells, releases an increased amount of EVs into the CSF in response to peripheral inflammation. Here, we studied the importance of CP-mediated EV release in AD pathogenesis. We observed increased EV levels in the CSF of young transgenic APP/PS1 mice which correlated with high amyloid beta (Aβ) CSF levels at this age. The intracerebroventricular (icv) injection of Aβ oligomers (AβO) in wild-type mice revealed a significant increase of EVs in the CSF, signifying that the presence of CSF-AβO is sufficient to induce increased EV secretion. Using in vivo, in vitro and ex vivo approaches, we identified the CP as a major source of the CSF-EVs. Interestingly, AβO-induced, CP-derived EVs induced pro-inflammatory effects in mixed cortical cultures. Proteome analysis of these EVs revealed the presence of several pro-inflammatory proteins, including the complement protein C3. Strikingly, inhibition of EV production using GW4869 resulted in protection against acute AβO-induced cognitive decline. Further research into the underlying mechanisms of this EV secretion might open up novel therapeutic strategies to impact the pathogenesis and progression of AD.",
journal = "Acta Neuropathologica Communications",
title = "Importance of extracellular vesicle secretion at the blood-cerebrospinal fluid interface in the pathogenesis of Alzheimer's disease.",
number = "1",
volume = "9",
doi = "10.1186/s40478-021-01245-z",
pages = "143"
}

Vandendriessche, C., Balusu, S., Van Cauwenberghe, C., Brkić, M., Pauwels, M., Plehiers, N., Bruggeman, A., Dujardin, P., Van Imschoot, G., Van Wonterghem, E., Hendrix, A., Baeke, F., De Rycke, R., Gevaert, K.,& Vandenbroucke, R. E.. (2021). Importance of extracellular vesicle secretion at the blood-cerebrospinal fluid interface in the pathogenesis of Alzheimer's disease.. in Acta Neuropathologica Communications, 9(1), 143.
https://doi.org/10.1186/s40478-021-01245-z

Vandendriessche C, Balusu S, Van Cauwenberghe C, Brkić M, Pauwels M, Plehiers N, Bruggeman A, Dujardin P, Van Imschoot G, Van Wonterghem E, Hendrix A, Baeke F, De Rycke R, Gevaert K, Vandenbroucke RE. Importance of extracellular vesicle secretion at the blood-cerebrospinal fluid interface in the pathogenesis of Alzheimer's disease.. in Acta Neuropathologica Communications. 2021;9(1):143.
doi:10.1186/s40478-021-01245-z .

Vandendriessche, Charysse, Balusu, Sriram, Van Cauwenberghe, Caroline, Brkić, Marjana, Pauwels, Marie, Plehiers, Nele, Bruggeman, Arnout, Dujardin, Pieter, Van Imschoot, Griet, Van Wonterghem, Elien, Hendrix, An, Baeke, Femke, De Rycke, Riet, Gevaert, Kris, Vandenbroucke, Roosmarijn E., "Importance of extracellular vesicle secretion at the blood-cerebrospinal fluid interface in the pathogenesis of Alzheimer's disease." in Acta Neuropathologica Communications, 9, no. 1 (2021):143,
https://doi.org/10.1186/s40478-021-01245-z . .

TY  - JOUR
AU  - Avramović, Vladimir
AU  - Frederiksen, Simona Denise
AU  - Brkić, Marjana
AU  - Tarailo-Graovac, Maja
PY  - 2021
UR  - https://humgenomics.biomedcentral.com/articles/10.1186/s40246-021-00371-y
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC8670043
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4756
AB  - BACKGROUND Genetic variation databases provide invaluable information on the presence and frequency of genetic variants in the 'untargeted' human population, aggregated with the primary goal to facilitate the interpretation of clinically important variants. The presence of somatic variants in such databases can affect variant assessment in undiagnosed rare disease (RD) patients. Previously, the impact of somatic mosaicism was only considered in relation to two Mendelian disease-associated genes. Here, we expand the analyses to identify additional mosaicism-prone genes in blood-derived reference population databases. RESULTS To identify additional mosaicism-prone genes relevant to RDs, we focused on known/previously established ClinVar pathogenic and likely pathogenic single-nucleotide variants, residing in genes associated with early onset, severe autosomal dominant diseases. We asked whether any of these variants are present in a higher-than-expected frequency in the reference population databases and whether there is evidence of somatic origin (i.e., allelic imbalance) rather than germline heterozygosity (~ half of the reads supporting alternative allele). The mosaicism-prone genes identified were further categorized according to the processes they are involved in. Beyond the previously reported ASXL1 and DNMT3A, we identified 7 additional autosomal dominant RD-associated genes with known pathogenic single-nucleotide variants present in the reference population databases and good evidence of allelic imbalance: BRAF, CBL, FGFR3, IDH2, KRAS, PTPN11 and SETBP1. From this group of 9 genes, the majority (n = 7) was important for hematopoiesis. In addition, 4 of these genes were involved in cell proliferation. Further assessment of the known 156 hematopoietic genes led to identification of 48 genes (21 not yet associated with RDs) with at least some evidence of mosaicism detectable in reference population databases. CONCLUSIONS These results stress the importance of considering genes involved in hematopoiesis and cell proliferation when interpreting the presence and frequency of genetic variants in blood-derived reference population databases, both public and private. This is especially important when considering new variants of uncertain significance in known hematopoietic/cell proliferation RD genes and future novel gene-disease associations involving this class of genes.
PB  - London: BioMed Central Ltd
T2  - Human Genomics
T1  - Driving mosaicism: somatic variants in reference population databases and effect on variant interpretation in rare genetic disease.
IS  - 1
VL  - 15
DO  - 10.1186/s40246-021-00371-y
SP  - 71
ER  - 

@article{
author = "Avramović, Vladimir and Frederiksen, Simona Denise and Brkić, Marjana and Tarailo-Graovac, Maja",
year = "2021",
abstract = "BACKGROUND Genetic variation databases provide invaluable information on the presence and frequency of genetic variants in the 'untargeted' human population, aggregated with the primary goal to facilitate the interpretation of clinically important variants. The presence of somatic variants in such databases can affect variant assessment in undiagnosed rare disease (RD) patients. Previously, the impact of somatic mosaicism was only considered in relation to two Mendelian disease-associated genes. Here, we expand the analyses to identify additional mosaicism-prone genes in blood-derived reference population databases. RESULTS To identify additional mosaicism-prone genes relevant to RDs, we focused on known/previously established ClinVar pathogenic and likely pathogenic single-nucleotide variants, residing in genes associated with early onset, severe autosomal dominant diseases. We asked whether any of these variants are present in a higher-than-expected frequency in the reference population databases and whether there is evidence of somatic origin (i.e., allelic imbalance) rather than germline heterozygosity (~ half of the reads supporting alternative allele). The mosaicism-prone genes identified were further categorized according to the processes they are involved in. Beyond the previously reported ASXL1 and DNMT3A, we identified 7 additional autosomal dominant RD-associated genes with known pathogenic single-nucleotide variants present in the reference population databases and good evidence of allelic imbalance: BRAF, CBL, FGFR3, IDH2, KRAS, PTPN11 and SETBP1. From this group of 9 genes, the majority (n = 7) was important for hematopoiesis. In addition, 4 of these genes were involved in cell proliferation. Further assessment of the known 156 hematopoietic genes led to identification of 48 genes (21 not yet associated with RDs) with at least some evidence of mosaicism detectable in reference population databases. CONCLUSIONS These results stress the importance of considering genes involved in hematopoiesis and cell proliferation when interpreting the presence and frequency of genetic variants in blood-derived reference population databases, both public and private. This is especially important when considering new variants of uncertain significance in known hematopoietic/cell proliferation RD genes and future novel gene-disease associations involving this class of genes.",
publisher = "London: BioMed Central Ltd",
journal = "Human Genomics",
title = "Driving mosaicism: somatic variants in reference population databases and effect on variant interpretation in rare genetic disease.",
number = "1",
volume = "15",
doi = "10.1186/s40246-021-00371-y",
pages = "71"
}

Avramović, V., Frederiksen, S. D., Brkić, M.,& Tarailo-Graovac, M.. (2021). Driving mosaicism: somatic variants in reference population databases and effect on variant interpretation in rare genetic disease.. in Human Genomics
London: BioMed Central Ltd., 15(1), 71.
https://doi.org/10.1186/s40246-021-00371-y

Avramović V, Frederiksen SD, Brkić M, Tarailo-Graovac M. Driving mosaicism: somatic variants in reference population databases and effect on variant interpretation in rare genetic disease.. in Human Genomics. 2021;15(1):71.
doi:10.1186/s40246-021-00371-y .

Avramović, Vladimir, Frederiksen, Simona Denise, Brkić, Marjana, Tarailo-Graovac, Maja, "Driving mosaicism: somatic variants in reference population databases and effect on variant interpretation in rare genetic disease." in Human Genomics, 15, no. 1 (2021):71,
https://doi.org/10.1186/s40246-021-00371-y . .

TY  - JOUR
AU  - Lazić, Divna
AU  - Tešić, Vesna
AU  - Jovanović, Mirna
AU  - Brkić, Marjana
AU  - Milanović, Desanka
AU  - Zloković, Berislav V.
AU  - Kanazir, Selma
AU  - Perović, Milka
PY  - 2020
UR  - http://www.ncbi.nlm.nih.gov/pubmed/31931140
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3596
AB  - Food restriction has been widely associated with beneficial effects on brain aging and age-related neurodegenerative diseases such as Alzheimer's disease. However, previous studies on the effects of food restriction on aging- or pathology-related cognitive decline are controversial, emphasizing the importance of the type, onset and duration of food restriction. In the present study, we assessed the effects of preventive every-other-day (EOD) feeding regimen on neurodegenerative phenotype in 5XFAD transgenic mice, a commonly used mouse model of Alzheimer's disease. EOD feeding regimen was introduced to transgenic female mice at the age of 2 months and the effects on amyloid-β (Aβ) accumulation, gliosis, synaptic plasticity, and blood-brain barrier breakdown were analyzed in cortical tissue of 6-month-old animals. Surprisingly, significant increase of inflammation in the cortex of 5XFAD fed EOD mice was observed, reflected by the expression of microglial and astrocytic markers. This increase in reactivity and/or proliferation of glial cells was accompanied by an increase in proinflammatory cytokine TNF-α, p38 MAPK and EAAT2, and a decrease in GAD67. NMDA receptor subunit 2B, related to glutamate excitotoxicity, was increased in the cortex of 5XFAD-EOD mice indicating additional alterations in glutamatergic signaling. Furthermore, 4 months of EOD feeding regimen had led to synaptic plasticity proteins reduction and neuronal injury in 5XFAD mice. However, EOD feeding regimen did not affect Aβ load and blood-brain barrier permeability in the cortex of 5XFAD mice. Our results demonstrate that EOD feeding regimen exacerbates Alzheimer's disease-like neurodegenerative and neuroinflammatory changes irrespective of Aβ pathology in 5XFAD mice, suggesting that caution should be paid when using food restrictions in the prodromal phase of this neurodegenerative disease.
T2  - Neurobiology of Disease
T1  - Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease.
VL  - 136
DO  - 10.1016/j.nbd.2020.104745
SP  - 104745
ER  - 

@article{
author = "Lazić, Divna and Tešić, Vesna and Jovanović, Mirna and Brkić, Marjana and Milanović, Desanka and Zloković, Berislav V. and Kanazir, Selma and Perović, Milka",
year = "2020",
abstract = "Food restriction has been widely associated with beneficial effects on brain aging and age-related neurodegenerative diseases such as Alzheimer's disease. However, previous studies on the effects of food restriction on aging- or pathology-related cognitive decline are controversial, emphasizing the importance of the type, onset and duration of food restriction. In the present study, we assessed the effects of preventive every-other-day (EOD) feeding regimen on neurodegenerative phenotype in 5XFAD transgenic mice, a commonly used mouse model of Alzheimer's disease. EOD feeding regimen was introduced to transgenic female mice at the age of 2 months and the effects on amyloid-β (Aβ) accumulation, gliosis, synaptic plasticity, and blood-brain barrier breakdown were analyzed in cortical tissue of 6-month-old animals. Surprisingly, significant increase of inflammation in the cortex of 5XFAD fed EOD mice was observed, reflected by the expression of microglial and astrocytic markers. This increase in reactivity and/or proliferation of glial cells was accompanied by an increase in proinflammatory cytokine TNF-α, p38 MAPK and EAAT2, and a decrease in GAD67. NMDA receptor subunit 2B, related to glutamate excitotoxicity, was increased in the cortex of 5XFAD-EOD mice indicating additional alterations in glutamatergic signaling. Furthermore, 4 months of EOD feeding regimen had led to synaptic plasticity proteins reduction and neuronal injury in 5XFAD mice. However, EOD feeding regimen did not affect Aβ load and blood-brain barrier permeability in the cortex of 5XFAD mice. Our results demonstrate that EOD feeding regimen exacerbates Alzheimer's disease-like neurodegenerative and neuroinflammatory changes irrespective of Aβ pathology in 5XFAD mice, suggesting that caution should be paid when using food restrictions in the prodromal phase of this neurodegenerative disease.",
journal = "Neurobiology of Disease",
title = "Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease.",
volume = "136",
doi = "10.1016/j.nbd.2020.104745",
pages = "104745"
}

Lazić, D., Tešić, V., Jovanović, M., Brkić, M., Milanović, D., Zloković, B. V., Kanazir, S.,& Perović, M.. (2020). Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease.. in Neurobiology of Disease, 136, 104745.
https://doi.org/10.1016/j.nbd.2020.104745

Lazić D, Tešić V, Jovanović M, Brkić M, Milanović D, Zloković BV, Kanazir S, Perović M. Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease.. in Neurobiology of Disease. 2020;136:104745.
doi:10.1016/j.nbd.2020.104745 .

Lazić, Divna, Tešić, Vesna, Jovanović, Mirna, Brkić, Marjana, Milanović, Desanka, Zloković, Berislav V., Kanazir, Selma, Perović, Milka, "Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease." in Neurobiology of Disease, 136 (2020):104745,
https://doi.org/10.1016/j.nbd.2020.104745 . .

TY  - JOUR
AU  - Steeland, Sophie
AU  - Gorlé, Nina
AU  - Vandendriessche, Charysse
AU  - Balusu, Sriram
AU  - Brkić, Marjana
AU  - Van Cauwenberghe, Caroline
AU  - Van Imschoot, Griet
AU  - Van Wonterghem, Elien
AU  - De Rycke, Riet
AU  - Kremer, Anneke
AU  - Lippens, Saskia
AU  - Stopa, Edward
AU  - Johanson, Conrad E
AU  - Libert, Claude
AU  - Vandenbroucke, Roosmarijn E
PY  - 2018
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29472246
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3005
AB  - Alzheimer's disease (AD) is the most common form of dementia, and neuroinflammation is an important hallmark of the pathogenesis. Tumor necrosis factor (TNF) might be detrimental in AD, though the results coming from clinical trials on anti-TNF inhibitors are inconclusive. TNFR1, one of the TNF signaling receptors, contributes to the pathogenesis of AD by mediating neuronal cell death. The blood-cerebrospinal fluid (CSF) barrier consists of a monolayer of choroid plexus epithelial (CPE) cells, and AD is associated with changes in CPE cell morphology. Here, we report that TNF is the main inflammatory upstream mediator in choroid plexus tissue in AD patients. This was confirmed in two murine AD models: transgenic APP/PS1 mice and intracerebroventricular (icv) AβO injection. TNFR1 contributes to the morphological damage of CPE cells in AD, and TNFR1 abrogation reduces brain inflammation and prevents blood-CSF barrier impairment. In APP/PS1 transgenic mice, TNFR1 deficiency ameliorated amyloidosis. Ultimately, genetic and pharmacological blockage of TNFR1 rescued from the induced cognitive impairments. Our data indicate that TNFR1 is a promising therapeutic target for AD treatment.
PB  - EMBO Press
T2  - EMBO Molecular Medicine
T1  - Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.
DO  - 10.15252/emmm.201708300
ER  - 

@article{
author = "Steeland, Sophie and Gorlé, Nina and Vandendriessche, Charysse and Balusu, Sriram and Brkić, Marjana and Van Cauwenberghe, Caroline and Van Imschoot, Griet and Van Wonterghem, Elien and De Rycke, Riet and Kremer, Anneke and Lippens, Saskia and Stopa, Edward and Johanson, Conrad E and Libert, Claude and Vandenbroucke, Roosmarijn E",
year = "2018",
abstract = "Alzheimer's disease (AD) is the most common form of dementia, and neuroinflammation is an important hallmark of the pathogenesis. Tumor necrosis factor (TNF) might be detrimental in AD, though the results coming from clinical trials on anti-TNF inhibitors are inconclusive. TNFR1, one of the TNF signaling receptors, contributes to the pathogenesis of AD by mediating neuronal cell death. The blood-cerebrospinal fluid (CSF) barrier consists of a monolayer of choroid plexus epithelial (CPE) cells, and AD is associated with changes in CPE cell morphology. Here, we report that TNF is the main inflammatory upstream mediator in choroid plexus tissue in AD patients. This was confirmed in two murine AD models: transgenic APP/PS1 mice and intracerebroventricular (icv) AβO injection. TNFR1 contributes to the morphological damage of CPE cells in AD, and TNFR1 abrogation reduces brain inflammation and prevents blood-CSF barrier impairment. In APP/PS1 transgenic mice, TNFR1 deficiency ameliorated amyloidosis. Ultimately, genetic and pharmacological blockage of TNFR1 rescued from the induced cognitive impairments. Our data indicate that TNFR1 is a promising therapeutic target for AD treatment.",
publisher = "EMBO Press",
journal = "EMBO Molecular Medicine",
title = "Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.",
doi = "10.15252/emmm.201708300"
}

Steeland, S., Gorlé, N., Vandendriessche, C., Balusu, S., Brkić, M., Van Cauwenberghe, C., Van Imschoot, G., Van Wonterghem, E., De Rycke, R., Kremer, A., Lippens, S., Stopa, E., Johanson, C. E., Libert, C.,& Vandenbroucke, R. E.. (2018). Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.. in EMBO Molecular Medicine
EMBO Press..
https://doi.org/10.15252/emmm.201708300

Steeland S, Gorlé N, Vandendriessche C, Balusu S, Brkić M, Van Cauwenberghe C, Van Imschoot G, Van Wonterghem E, De Rycke R, Kremer A, Lippens S, Stopa E, Johanson CE, Libert C, Vandenbroucke RE. Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease.. in EMBO Molecular Medicine. 2018;.
doi:10.15252/emmm.201708300 .

Steeland, Sophie, Gorlé, Nina, Vandendriessche, Charysse, Balusu, Sriram, Brkić, Marjana, Van Cauwenberghe, Caroline, Van Imschoot, Griet, Van Wonterghem, Elien, De Rycke, Riet, Kremer, Anneke, Lippens, Saskia, Stopa, Edward, Johanson, Conrad E, Libert, Claude, Vandenbroucke, Roosmarijn E, "Counteracting the effects of TNF receptor-1 has therapeutic potential in Alzheimer's disease." in EMBO Molecular Medicine (2018),
https://doi.org/10.15252/emmm.201708300 . .

TY  - JOUR
AU  - Milanović, Desanka
AU  - Petrovic, Snjezana
AU  - Brkić, Marjana
AU  - Avramović, Vladimir
AU  - Perović, Milka
AU  - Ivković, Sanja
AU  - Glibetić, Marija
AU  - Kanazir, Selma
PY  - 2018
UR  - http://www.mdpi.com/2072-6643/10/9/1250
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3136
AB  - Long-term fish oil (FO) supplementation is able to improve Alzheimer's disease (AD) pathology. We aimed to determine the impact of short-term fish oil (FO) intake on phospholipids composition and plaque pathology in 5xFAD mice, a widely used animal model of AD. A 3-week-long FO supplementation administered at 3 months of age decreased the number of dense core plaques in the 5xFAD cortex and changed phospholipids in the livers and brains of wild-type (Wt) and 5xFAD mice. Livers of both genotypes responded by increase of n-3 and reciprocal decrease of n-6 fatty acids. In Wt brains, FO supplementation induced elevation of n-3 fatty acids and subsequent enhancement of n-6/n-3 ratio. However, in 5xFAD brains the improved n-6/n-3 ratio was mainly due to FO-induced decrease in arachidonic and adrenic n-6 fatty acids. Also, brain and liver abundance of n-3 fatty acids were strongly correlated in Wts, oppositely to 5xFADs where significant brain-liver correlation exists only for n-6 fatty acids. Expression of omega-3 transporter Mfs2a remained unchanged after FO supplementation. We have demonstrated that even a short-term FO intake improves the phospholipid composition and has a significant effect on plaque burden in 5xFAD brains when applied in early stages of AD pathology.
T2  - Nutrients
T1  - Short-Term Fish Oil Treatment Changes the Composition of Phospholipids While Not Affecting the Expression of Mfsd2a Omega-3 Transporter in the Brain and Liver of the 5xFAD Mouse Model of Alzheimer's Disease.
IS  - 9
VL  - 10
DO  - 10.3390/nu10091250
SP  - 1250
ER  - 

@article{
author = "Milanović, Desanka and Petrovic, Snjezana and Brkić, Marjana and Avramović, Vladimir and Perović, Milka and Ivković, Sanja and Glibetić, Marija and Kanazir, Selma",
year = "2018",
abstract = "Long-term fish oil (FO) supplementation is able to improve Alzheimer's disease (AD) pathology. We aimed to determine the impact of short-term fish oil (FO) intake on phospholipids composition and plaque pathology in 5xFAD mice, a widely used animal model of AD. A 3-week-long FO supplementation administered at 3 months of age decreased the number of dense core plaques in the 5xFAD cortex and changed phospholipids in the livers and brains of wild-type (Wt) and 5xFAD mice. Livers of both genotypes responded by increase of n-3 and reciprocal decrease of n-6 fatty acids. In Wt brains, FO supplementation induced elevation of n-3 fatty acids and subsequent enhancement of n-6/n-3 ratio. However, in 5xFAD brains the improved n-6/n-3 ratio was mainly due to FO-induced decrease in arachidonic and adrenic n-6 fatty acids. Also, brain and liver abundance of n-3 fatty acids were strongly correlated in Wts, oppositely to 5xFADs where significant brain-liver correlation exists only for n-6 fatty acids. Expression of omega-3 transporter Mfs2a remained unchanged after FO supplementation. We have demonstrated that even a short-term FO intake improves the phospholipid composition and has a significant effect on plaque burden in 5xFAD brains when applied in early stages of AD pathology.",
journal = "Nutrients",
title = "Short-Term Fish Oil Treatment Changes the Composition of Phospholipids While Not Affecting the Expression of Mfsd2a Omega-3 Transporter in the Brain and Liver of the 5xFAD Mouse Model of Alzheimer's Disease.",
number = "9",
volume = "10",
doi = "10.3390/nu10091250",
pages = "1250"
}

Milanović, D., Petrovic, S., Brkić, M., Avramović, V., Perović, M., Ivković, S., Glibetić, M.,& Kanazir, S.. (2018). Short-Term Fish Oil Treatment Changes the Composition of Phospholipids While Not Affecting the Expression of Mfsd2a Omega-3 Transporter in the Brain and Liver of the 5xFAD Mouse Model of Alzheimer's Disease.. in Nutrients, 10(9), 1250.
https://doi.org/10.3390/nu10091250

Milanović D, Petrovic S, Brkić M, Avramović V, Perović M, Ivković S, Glibetić M, Kanazir S. Short-Term Fish Oil Treatment Changes the Composition of Phospholipids While Not Affecting the Expression of Mfsd2a Omega-3 Transporter in the Brain and Liver of the 5xFAD Mouse Model of Alzheimer's Disease.. in Nutrients. 2018;10(9):1250.
doi:10.3390/nu10091250 .

Milanović, Desanka, Petrovic, Snjezana, Brkić, Marjana, Avramović, Vladimir, Perović, Milka, Ivković, Sanja, Glibetić, Marija, Kanazir, Selma, "Short-Term Fish Oil Treatment Changes the Composition of Phospholipids While Not Affecting the Expression of Mfsd2a Omega-3 Transporter in the Brain and Liver of the 5xFAD Mouse Model of Alzheimer's Disease." in Nutrients, 10, no. 9 (2018):1250,
https://doi.org/10.3390/nu10091250 . .

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  - 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  - CONF
AU  - Avramović, Vladimir
AU  - Milanović, Desanka
AU  - Brkić, Marjana
AU  - Babić, Nikolina
AU  - Jović, Milena
AU  - Perović, Milka
AU  - Tešić, Vesna
AU  - Ivković, Sanja
AU  - Kanazir, Selma
PY  - 2016
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5829
AB  - Clinico-pathological features of Alzheimer's disease (AD) include memory loss, cognitive impairment, depression and social isolation. Epidemiological studies show a positive role of omega-3 poly-unsaturated fatty acids (n-3 PU FA) on prevention and mitigation of mild AD pathology. The 5xFAD mouse model used in this study bears five mutations linked to familiar forms of AD and recapitulates in a few months the main features of AD. This study was aimed to evaluate the effect of pre- and peri-natal omega-3 fatty acids supplementation on cognitive and non-cognitive behavior of 5xFAD mice . The fish oil, an abundant source of n-3 PUFA, was supplemented via oral gavages five days per week to dames throughout whole pregnancy and lactation. Six-month old offsprings were subjected to a battery of behavioral tests in order to assess typical rodent behavior, general locomotor activity, memory, depressive-like and social behavior. We have observed that the fish oil-supplemented 5xFAD offspring showed no changes in tests assessing typical rodent behavior, such as marble and nesting test, in comparison with 5XFAD control mice. When assessing depression and anxiety like behavior in a light-dark box, forced swim and open field behavioral tests significant changes were observed only between non-transgenic and transgenic mice. However, in three chambers test, used for assessing social behavior, fish oil- treated 5xFAD mice showed a significant increase in sociability, evaluated by increased time spent in compartment with, a mouse vs. empty compartment. Moreover, when the social novelty was tested through the introduction of a new mouse, the same trend was observed. This study shows that the pre- and peri-natal fish oil supplementation in 5xFAD mice can exert long-lasting effects inducing the significant improvement in some of the behavioral aspects of AD pathology in the adult offspring.
PB  - Belgrade: Serbian Nutrition Society
C3  - Book of Abstracts: 13th Congress of Nutrition Food and Nutrition: A Roadmap to Better Health; 2016 Oct 26-28; Belgrade, Serbia
T1  - Fish oil supplementation during pre- and peri-natal period: Behavioral phenotyping of transgenic mouse model of Alzheimer’s disease
SP  - 257
EP  - 258
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5829
ER  - 

@conference{
author = "Avramović, Vladimir and Milanović, Desanka and Brkić, Marjana and Babić, Nikolina and Jović, Milena and Perović, Milka and Tešić, Vesna and Ivković, Sanja and Kanazir, Selma",
year = "2016",
abstract = "Clinico-pathological features of Alzheimer's disease (AD) include memory loss, cognitive impairment, depression and social isolation. Epidemiological studies show a positive role of omega-3 poly-unsaturated fatty acids (n-3 PU FA) on prevention and mitigation of mild AD pathology. The 5xFAD mouse model used in this study bears five mutations linked to familiar forms of AD and recapitulates in a few months the main features of AD. This study was aimed to evaluate the effect of pre- and peri-natal omega-3 fatty acids supplementation on cognitive and non-cognitive behavior of 5xFAD mice . The fish oil, an abundant source of n-3 PUFA, was supplemented via oral gavages five days per week to dames throughout whole pregnancy and lactation. Six-month old offsprings were subjected to a battery of behavioral tests in order to assess typical rodent behavior, general locomotor activity, memory, depressive-like and social behavior. We have observed that the fish oil-supplemented 5xFAD offspring showed no changes in tests assessing typical rodent behavior, such as marble and nesting test, in comparison with 5XFAD control mice. When assessing depression and anxiety like behavior in a light-dark box, forced swim and open field behavioral tests significant changes were observed only between non-transgenic and transgenic mice. However, in three chambers test, used for assessing social behavior, fish oil- treated 5xFAD mice showed a significant increase in sociability, evaluated by increased time spent in compartment with, a mouse vs. empty compartment. Moreover, when the social novelty was tested through the introduction of a new mouse, the same trend was observed. This study shows that the pre- and peri-natal fish oil supplementation in 5xFAD mice can exert long-lasting effects inducing the significant improvement in some of the behavioral aspects of AD pathology in the adult offspring.",
publisher = "Belgrade: Serbian Nutrition Society",
journal = "Book of Abstracts: 13th Congress of Nutrition Food and Nutrition: A Roadmap to Better Health; 2016 Oct 26-28; Belgrade, Serbia",
title = "Fish oil supplementation during pre- and peri-natal period: Behavioral phenotyping of transgenic mouse model of Alzheimer’s disease",
pages = "257-258",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5829"
}

Avramović, V., Milanović, D., Brkić, M., Babić, N., Jović, M., Perović, M., Tešić, V., Ivković, S.,& Kanazir, S.. (2016). Fish oil supplementation during pre- and peri-natal period: Behavioral phenotyping of transgenic mouse model of Alzheimer’s disease. in Book of Abstracts: 13th Congress of Nutrition Food and Nutrition: A Roadmap to Better Health; 2016 Oct 26-28; Belgrade, Serbia
Belgrade: Serbian Nutrition Society., 257-258.
https://hdl.handle.net/21.15107/rcub_ibiss_5829

Avramović V, Milanović D, Brkić M, Babić N, Jović M, Perović M, Tešić V, Ivković S, Kanazir S. Fish oil supplementation during pre- and peri-natal period: Behavioral phenotyping of transgenic mouse model of Alzheimer’s disease. in Book of Abstracts: 13th Congress of Nutrition Food and Nutrition: A Roadmap to Better Health; 2016 Oct 26-28; Belgrade, Serbia. 2016;:257-258.
https://hdl.handle.net/21.15107/rcub_ibiss_5829 .

Avramović, Vladimir, Milanović, Desanka, Brkić, Marjana, Babić, Nikolina, Jović, Milena, Perović, Milka, Tešić, Vesna, Ivković, Sanja, Kanazir, Selma, "Fish oil supplementation during pre- and peri-natal period: Behavioral phenotyping of transgenic mouse model of Alzheimer’s disease" in Book of Abstracts: 13th Congress of Nutrition Food and Nutrition: A Roadmap to Better Health; 2016 Oct 26-28; Belgrade, Serbia (2016):257-258,
https://hdl.handle.net/21.15107/rcub_ibiss_5829 .

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  - Balusu, Sriram
AU  - Van Wonterghem, Elien
AU  - De Rycke, Riet
AU  - Raemdonck, Koen
AU  - Stremersch, Stephan
AU  - Gevaert, Kris
AU  - Brkić, Marjana
AU  - Demeestere, Delphine
AU  - Vanhooren, Valerie
AU  - Hendrix, An
AU  - Libert, Claude
AU  - Vandenbroucke, Roosmarijn E.
PY  - 2016
UR  - http://embomolmed.embopress.org/lookup/doi/10.15252/emmm.201606271
UR  - https://www.scopus.com/record/display.uri?eid=2-s2.0-84989915450&origin=SingleRecordEmailAlert&txGid=66B9A38F509F4540CF41E07DD21FB6C0.wsnAw8kcdt7IPYLO0V48gA:27#
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2471
AB  - Here, we identified release of extracellular vesicles (EVs) by the choroid plexus epithelium (CPE) as a new mechanism of blood–brain communication. Systemic inflammation induced an increase in EVs and associated pro-inflammatory miRNAs, including miR-146a and miR-155, in the CSF. Interestingly, this was associated with an increase in amount of multivesicular bodies (MVBs) and exosomes per MVB in the CPE cells. Additionally, we could mimic this using LPS-stimulated primary CPE cells and choroid plexus explants. These choroid plexus-derived EVs can enter the brain parenchyma and are taken up by astrocytes and microglia, inducing miRNA target repression and inflammatory gene up-regulation. Interestingly, this could be blocked in vivo by intracerebroventricular (icv) injection of an inhibitor of exosome production. Our data show that CPE cells sense and transmit information about the peripheral inflammatory status to the central nervous system (CNS) via the release of EVs into the CSF, which transfer this pro-inflammatory message to recipient brain cells. Additionally, we revealed that blockage of EV secretion decreases brain inflammation, which opens up new avenues to treat systemic inflammatory diseases such as sepsis.
PB  - Blackwell Publishing Ltd
T2  - EMBO Molecular Medicine
T1  - Identification of a novel mechanism of blood–brain communication during peripheral inflammation via choroid plexus‐derived extracellular vesicles
IS  - 10
VL  - 8
DO  - 10.15252/emmm.201606271
SP  - 1162
EP  - 1183
ER  - 

@article{
author = "Balusu, Sriram and Van Wonterghem, Elien and De Rycke, Riet and Raemdonck, Koen and Stremersch, Stephan and Gevaert, Kris and Brkić, Marjana and Demeestere, Delphine and Vanhooren, Valerie and Hendrix, An and Libert, Claude and Vandenbroucke, Roosmarijn E.",
year = "2016",
abstract = "Here, we identified release of extracellular vesicles (EVs) by the choroid plexus epithelium (CPE) as a new mechanism of blood–brain communication. Systemic inflammation induced an increase in EVs and associated pro-inflammatory miRNAs, including miR-146a and miR-155, in the CSF. Interestingly, this was associated with an increase in amount of multivesicular bodies (MVBs) and exosomes per MVB in the CPE cells. Additionally, we could mimic this using LPS-stimulated primary CPE cells and choroid plexus explants. These choroid plexus-derived EVs can enter the brain parenchyma and are taken up by astrocytes and microglia, inducing miRNA target repression and inflammatory gene up-regulation. Interestingly, this could be blocked in vivo by intracerebroventricular (icv) injection of an inhibitor of exosome production. Our data show that CPE cells sense and transmit information about the peripheral inflammatory status to the central nervous system (CNS) via the release of EVs into the CSF, which transfer this pro-inflammatory message to recipient brain cells. Additionally, we revealed that blockage of EV secretion decreases brain inflammation, which opens up new avenues to treat systemic inflammatory diseases such as sepsis.",
publisher = "Blackwell Publishing Ltd",
journal = "EMBO Molecular Medicine",
title = "Identification of a novel mechanism of blood–brain communication during peripheral inflammation via choroid plexus‐derived extracellular vesicles",
number = "10",
volume = "8",
doi = "10.15252/emmm.201606271",
pages = "1162-1183"
}

Balusu, S., Van Wonterghem, E., De Rycke, R., Raemdonck, K., Stremersch, S., Gevaert, K., Brkić, M., Demeestere, D., Vanhooren, V., Hendrix, A., Libert, C.,& Vandenbroucke, R. E.. (2016). Identification of a novel mechanism of blood–brain communication during peripheral inflammation via choroid plexus‐derived extracellular vesicles. in EMBO Molecular Medicine
Blackwell Publishing Ltd., 8(10), 1162-1183.
https://doi.org/10.15252/emmm.201606271

Balusu S, Van Wonterghem E, De Rycke R, Raemdonck K, Stremersch S, Gevaert K, Brkić M, Demeestere D, Vanhooren V, Hendrix A, Libert C, Vandenbroucke RE. Identification of a novel mechanism of blood–brain communication during peripheral inflammation via choroid plexus‐derived extracellular vesicles. in EMBO Molecular Medicine. 2016;8(10):1162-1183.
doi:10.15252/emmm.201606271 .

Balusu, Sriram, Van Wonterghem, Elien, De Rycke, Riet, Raemdonck, Koen, Stremersch, Stephan, Gevaert, Kris, Brkić, Marjana, Demeestere, Delphine, Vanhooren, Valerie, Hendrix, An, Libert, Claude, Vandenbroucke, Roosmarijn E., "Identification of a novel mechanism of blood–brain communication during peripheral inflammation via choroid plexus‐derived extracellular vesicles" in EMBO Molecular Medicine, 8, no. 10 (2016):1162-1183,
https://doi.org/10.15252/emmm.201606271 . .

TY  - JOUR
AU  - Smiljanić, Kosara
AU  - Pesic, Vesna
AU  - Mladenović, Aleksandra
AU  - Pavković, Željko
AU  - Brkić, Marjana
AU  - Ruždijić, Sabera
AU  - Kanazir, Selma
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2013
AB  - Dietary restriction (DR) exerts significant beneficial effects in terms
   of aging and age-related diseases in many organisms including humans.
   The present study aimed to examine the influence of long-term DR on the
   BDNF system at the transcriptional and translational levels in the
   cortex and hippocampus of middle-aged (12-month-old) and aged
   (24-month-old) male Wistar rats. The obtained results revealed that the
   DR upregulated the expression of exon-specific BDNF transcripts in both
   regions, followed by elevated levels of mBDNF only in the cortex in
   middle-aged animals. In aged animals, DR modulated BDNF protein levels
   by increasing proBDNF and by declining mBDNF levels. Additionally,
   elevated levels of the full-length TrkB accompanied by a decreased level
   of the less-glycosylated TrkB protein were observed in middle-aged rats
   following DR, while in aged rats, DR amplified only the expression of
   the less-glycosylated form of TrkB. The levels of phosphorylated
   TrkB(Y816) were stable during aging regardless of feeding. Reduced
   levels of p75(NTR) were detected in both regions of middle-aged DR-fed
   animals, while a significant increase was measured in the cortex of aged
   DR-fed rats. These findings shed additional light on DR as a modulator
   of BDNF system revealing its disparate effects in middle-aged and aged
   animals. Given the importance of the proBDNF/BDNF circuit-level
   expression in different brain functions and various aspects of behavior,
   it is necessary to further elucidate the optimal duration of the applied
   dietary regimen with regard to the animal age in order to achieve its
   most favorable effects.
T2  - Biogerontology
T1  - Long-term dietary restriction differentially affects the expression of
 BDNF and its receptors in the cortex and hippocampus of middle-aged and
 aged male rats
IS  - 1
VL  - 16
DO  - 10.1007/s10522-014-9537-9
SP  - 71
EP  - 83
ER  - 

@article{
author = "Smiljanić, Kosara and Pesic, Vesna and Mladenović, Aleksandra and Pavković, Željko and Brkić, Marjana and Ruždijić, Sabera and Kanazir, Selma",
year = "2015",
abstract = "Dietary restriction (DR) exerts significant beneficial effects in terms
   of aging and age-related diseases in many organisms including humans.
   The present study aimed to examine the influence of long-term DR on the
   BDNF system at the transcriptional and translational levels in the
   cortex and hippocampus of middle-aged (12-month-old) and aged
   (24-month-old) male Wistar rats. The obtained results revealed that the
   DR upregulated the expression of exon-specific BDNF transcripts in both
   regions, followed by elevated levels of mBDNF only in the cortex in
   middle-aged animals. In aged animals, DR modulated BDNF protein levels
   by increasing proBDNF and by declining mBDNF levels. Additionally,
   elevated levels of the full-length TrkB accompanied by a decreased level
   of the less-glycosylated TrkB protein were observed in middle-aged rats
   following DR, while in aged rats, DR amplified only the expression of
   the less-glycosylated form of TrkB. The levels of phosphorylated
   TrkB(Y816) were stable during aging regardless of feeding. Reduced
   levels of p75(NTR) were detected in both regions of middle-aged DR-fed
   animals, while a significant increase was measured in the cortex of aged
   DR-fed rats. These findings shed additional light on DR as a modulator
   of BDNF system revealing its disparate effects in middle-aged and aged
   animals. Given the importance of the proBDNF/BDNF circuit-level
   expression in different brain functions and various aspects of behavior,
   it is necessary to further elucidate the optimal duration of the applied
   dietary regimen with regard to the animal age in order to achieve its
   most favorable effects.",
journal = "Biogerontology",
title = "Long-term dietary restriction differentially affects the expression of
 BDNF and its receptors in the cortex and hippocampus of middle-aged and
 aged male rats",
number = "1",
volume = "16",
doi = "10.1007/s10522-014-9537-9",
pages = "71-83"
}

Smiljanić, K., Pesic, V., Mladenović, A., Pavković, Ž., Brkić, M., Ruždijić, S.,& Kanazir, S.. (2015). Long-term dietary restriction differentially affects the expression of
 BDNF and its receptors in the cortex and hippocampus of middle-aged and
 aged male rats. in Biogerontology, 16(1), 71-83.
https://doi.org/10.1007/s10522-014-9537-9

Smiljanić K, Pesic V, Mladenović A, Pavković Ž, Brkić M, Ruždijić S, Kanazir S. Long-term dietary restriction differentially affects the expression of
 BDNF and its receptors in the cortex and hippocampus of middle-aged and
 aged male rats. in Biogerontology. 2015;16(1):71-83.
doi:10.1007/s10522-014-9537-9 .

Smiljanić, Kosara, Pesic, Vesna, Mladenović, Aleksandra, Pavković, Željko, Brkić, Marjana, Ruždijić, Sabera, Kanazir, Selma, "Long-term dietary restriction differentially affects the expression of
 BDNF and its receptors in the cortex and hippocampus of middle-aged and
 aged male rats" in Biogerontology, 16, no. 1 (2015):71-83,
https://doi.org/10.1007/s10522-014-9537-9 . .