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 . .

TY  - JOUR
AU  - Tesic, Vesna
AU  - Perovic, Milka
AU  - Lazic, Divna
AU  - Kojic, Snezana
AU  - Smiljanić, Kosara
AU  - Ruždijić, Sabera
AU  - Rakic, Ljubisav
AU  - Kanazir, Selma
PY  - 2015
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1967
AB  - Diminished glucocorticoid signaling is associated with an age-related
   decline in hippocampal functioning. In this study we demonstrate the
   effect of intermittent, every other day (EOD) feeding on the
   glucocorticoid hormone/glucocorticoid receptor (GR) system in the
   hippocampus of middle-aged (18-month-old) and aged (24-month-old) Wistar
   rats. In aged ad libitum-fed rats, a decrease in the level of total GR
   and GR phosphorylated at Ser(232) (pGR) was detected. Conversely, aged
   rats subjected to EOD feeding, starting from 6 months of age, showed an
   increase in GR and pGR levels and a higher content of hippocampal
   corticosterone. Furthermore, prominent nuclear staining of pGR was
   observed in CM pyramidal and DG granule neurons of aged EOD-fed rats.
   These changes were accompanied by increased Sglc-1 and decreased GFAP
   transcription, pointing to upregulated transcriptional activity of GR.
   EOD feeding also induced an increase in the expression of the
   mineralocorticoid receptor. Our results reveal that intermittent feeding
   restores impaired GR signaling in the hippocampus of aged animals by
   inducing rather than by stabilizing GR signaling during aging. (C) 2015
   Elsevier Ltd. All rights reserved.
T2  - Journal of Steroid Biochemistry and Molecular Biology
T1  - Long-term intermittent feeding restores impaired GR signaling in the
 hippocampus of aged rat
VL  - 149
DO  - 10.1016/j.jsbmb.2015.01.013
SP  - 43
EP  - 52
ER  - 

@article{
author = "Tesic, Vesna and Perovic, Milka and Lazic, Divna and Kojic, Snezana and Smiljanić, Kosara and Ruždijić, Sabera and Rakic, Ljubisav and Kanazir, Selma",
year = "2015",
abstract = "Diminished glucocorticoid signaling is associated with an age-related
   decline in hippocampal functioning. In this study we demonstrate the
   effect of intermittent, every other day (EOD) feeding on the
   glucocorticoid hormone/glucocorticoid receptor (GR) system in the
   hippocampus of middle-aged (18-month-old) and aged (24-month-old) Wistar
   rats. In aged ad libitum-fed rats, a decrease in the level of total GR
   and GR phosphorylated at Ser(232) (pGR) was detected. Conversely, aged
   rats subjected to EOD feeding, starting from 6 months of age, showed an
   increase in GR and pGR levels and a higher content of hippocampal
   corticosterone. Furthermore, prominent nuclear staining of pGR was
   observed in CM pyramidal and DG granule neurons of aged EOD-fed rats.
   These changes were accompanied by increased Sglc-1 and decreased GFAP
   transcription, pointing to upregulated transcriptional activity of GR.
   EOD feeding also induced an increase in the expression of the
   mineralocorticoid receptor. Our results reveal that intermittent feeding
   restores impaired GR signaling in the hippocampus of aged animals by
   inducing rather than by stabilizing GR signaling during aging. (C) 2015
   Elsevier Ltd. All rights reserved.",
journal = "Journal of Steroid Biochemistry and Molecular Biology",
title = "Long-term intermittent feeding restores impaired GR signaling in the
 hippocampus of aged rat",
volume = "149",
doi = "10.1016/j.jsbmb.2015.01.013",
pages = "43-52"
}

Tesic, V., Perovic, M., Lazic, D., Kojic, S., Smiljanić, K., Ruždijić, S., Rakic, L.,& Kanazir, S.. (2015). Long-term intermittent feeding restores impaired GR signaling in the
 hippocampus of aged rat. in Journal of Steroid Biochemistry and Molecular Biology, 149, 43-52.
https://doi.org/10.1016/j.jsbmb.2015.01.013

Tesic V, Perovic M, Lazic D, Kojic S, Smiljanić K, Ruždijić S, Rakic L, Kanazir S. Long-term intermittent feeding restores impaired GR signaling in the
 hippocampus of aged rat. in Journal of Steroid Biochemistry and Molecular Biology. 2015;149:43-52.
doi:10.1016/j.jsbmb.2015.01.013 .

Tesic, Vesna, Perovic, Milka, Lazic, Divna, Kojic, Snezana, Smiljanić, Kosara, Ruždijić, Sabera, Rakic, Ljubisav, Kanazir, Selma, "Long-term intermittent feeding restores impaired GR signaling in the
 hippocampus of aged rat" in Journal of Steroid Biochemistry and Molecular Biology, 149 (2015):43-52,
https://doi.org/10.1016/j.jsbmb.2015.01.013 . .