Zloković, Berislav

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eb397266-386c-45f5-99c3-1cf169b8f94c
  • Zloković, Berislav (1)
  • Zlokovic, Berislav V (1)
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Author's Bibliography

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.

Jović, Milena; Lončarević-Vasiljković, Nataša; Ivković, Sanja; Dinić, Jelena; Milanović, Desanka; Zloković, Berislav; Kanazir, Selma

(2019)

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 . .
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Pericyte degeneration causes white matter dysfunction in the mouse central nervous system.

Montagne, Axel; Nikolakopoulou, Angeliki M; Zhao, Zhen; Sagare, Abhay P; Si, Gabriel; Lazic, Divna; Barnes, Samuel R; Daianu, Madelaine; Ramanathan, Anita; Go, Ariel; Lawson, Erica J; Wang, Yaoming; Mack, William J; Thompson, Paul M; Schneider, Julie A; Varkey, Jobin; Langen, Ralf; Mullins, Eric; Jacobs, Russell E; Zlokovic, Berislav V

(2018)

TY  - JOUR
AU  - Montagne, Axel
AU  - Nikolakopoulou, Angeliki M
AU  - Zhao, Zhen
AU  - Sagare, Abhay P
AU  - Si, Gabriel
AU  - Lazic, Divna
AU  - Barnes, Samuel R
AU  - Daianu, Madelaine
AU  - Ramanathan, Anita
AU  - Go, Ariel
AU  - Lawson, Erica J
AU  - Wang, Yaoming
AU  - Mack, William J
AU  - Thompson, Paul M
AU  - Schneider, Julie A
AU  - Varkey, Jobin
AU  - Langen, Ralf
AU  - Mullins, Eric
AU  - Jacobs, Russell E
AU  - Zlokovic, Berislav V
PY  - 2018
UR  - http://www.nature.com/doifinder/10.1038/nm.4482
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC5840035
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3012
AB  - Diffuse white-matter disease associated with small-vessel disease and dementia is prevalent in the elderly. The biological mechanisms, however, remain elusive. Using pericyte-deficient mice, magnetic resonance imaging, viral-based tract-tracing, and behavior and tissue analysis, we found that pericyte degeneration disrupted white-matter microcirculation, resulting in an accumulation of toxic blood-derived fibrin(ogen) deposits and blood-flow reductions, which triggered a loss of myelin, axons and oligodendrocytes. This disrupted brain circuits, leading to white-matter functional deficits before neuronal loss occurs. Fibrinogen and fibrin fibrils initiated autophagy-dependent cell death in oligodendrocyte and pericyte cultures, whereas pharmacological and genetic manipulations of systemic fibrinogen levels in pericyte-deficient, but not control mice, influenced the degree of white-matter fibrin(ogen) deposition, pericyte degeneration, vascular pathology and white-matter changes. Thus, our data indicate that pericytes control white-matter structure and function, which has implications for the pathogenesis and treatment of human white-matter disease associated with small-vessel disease.
T2  - Nature Medicine
T2  - Nature Medicine
T1  - Pericyte degeneration causes white matter dysfunction in the mouse central nervous system.
IS  - 3
VL  - 24
DO  - 10.1038/nm.4482
SP  - 326
EP  - 337
ER  - 
@article{
author = "Montagne, Axel and Nikolakopoulou, Angeliki M and Zhao, Zhen and Sagare, Abhay P and Si, Gabriel and Lazic, Divna and Barnes, Samuel R and Daianu, Madelaine and Ramanathan, Anita and Go, Ariel and Lawson, Erica J and Wang, Yaoming and Mack, William J and Thompson, Paul M and Schneider, Julie A and Varkey, Jobin and Langen, Ralf and Mullins, Eric and Jacobs, Russell E and Zlokovic, Berislav V",
year = "2018",
abstract = "Diffuse white-matter disease associated with small-vessel disease and dementia is prevalent in the elderly. The biological mechanisms, however, remain elusive. Using pericyte-deficient mice, magnetic resonance imaging, viral-based tract-tracing, and behavior and tissue analysis, we found that pericyte degeneration disrupted white-matter microcirculation, resulting in an accumulation of toxic blood-derived fibrin(ogen) deposits and blood-flow reductions, which triggered a loss of myelin, axons and oligodendrocytes. This disrupted brain circuits, leading to white-matter functional deficits before neuronal loss occurs. Fibrinogen and fibrin fibrils initiated autophagy-dependent cell death in oligodendrocyte and pericyte cultures, whereas pharmacological and genetic manipulations of systemic fibrinogen levels in pericyte-deficient, but not control mice, influenced the degree of white-matter fibrin(ogen) deposition, pericyte degeneration, vascular pathology and white-matter changes. Thus, our data indicate that pericytes control white-matter structure and function, which has implications for the pathogenesis and treatment of human white-matter disease associated with small-vessel disease.",
journal = "Nature Medicine, Nature Medicine",
title = "Pericyte degeneration causes white matter dysfunction in the mouse central nervous system.",
number = "3",
volume = "24",
doi = "10.1038/nm.4482",
pages = "326-337"
}
Montagne, A., Nikolakopoulou, A. M., Zhao, Z., Sagare, A. P., Si, G., Lazic, D., Barnes, S. R., Daianu, M., Ramanathan, A., Go, A., Lawson, E. J., Wang, Y., Mack, W. J., Thompson, P. M., Schneider, J. A., Varkey, J., Langen, R., Mullins, E., Jacobs, R. E.,& Zlokovic, B. V.. (2018). Pericyte degeneration causes white matter dysfunction in the mouse central nervous system.. in Nature Medicine, 24(3), 326-337.
https://doi.org/10.1038/nm.4482
Montagne A, Nikolakopoulou AM, Zhao Z, Sagare AP, Si G, Lazic D, Barnes SR, Daianu M, Ramanathan A, Go A, Lawson EJ, Wang Y, Mack WJ, Thompson PM, Schneider JA, Varkey J, Langen R, Mullins E, Jacobs RE, Zlokovic BV. Pericyte degeneration causes white matter dysfunction in the mouse central nervous system.. in Nature Medicine. 2018;24(3):326-337.
doi:10.1038/nm.4482 .
Montagne, Axel, Nikolakopoulou, Angeliki M, Zhao, Zhen, Sagare, Abhay P, Si, Gabriel, Lazic, Divna, Barnes, Samuel R, Daianu, Madelaine, Ramanathan, Anita, Go, Ariel, Lawson, Erica J, Wang, Yaoming, Mack, William J, Thompson, Paul M, Schneider, Julie A, Varkey, Jobin, Langen, Ralf, Mullins, Eric, Jacobs, Russell E, Zlokovic, Berislav V, "Pericyte degeneration causes white matter dysfunction in the mouse central nervous system." in Nature Medicine, 24, no. 3 (2018):326-337,
https://doi.org/10.1038/nm.4482 . .
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