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https://www.readbyqxmd.com/read/27558169/activation-of-microglia-by-retroviral-infection-correlate-with-transient-clearance-of-prions-from-the-brain-but-does-not-change-incubation-time
#1
Christiane Muth, Katharina Schröck, Charlotte Madore, Kristin Hartmann, Zain Fanek, Oleg Butovsky, Markus Glatzel, Susanne Krasemann
Prion diseases are fatal transmissible diseases, where conversion of the endogenous prion protein (PrP(C) ) into a misfolded isoform (PrP(Sc) ) leads to neurodegeneration. Microglia, the immune cells of the brain, are activated in neurodegenerative disorders including prion diseases, however their impact on prion disease pathophysiology is unclear with both beneficial PrP(Sc) -clearing and detrimental potentially neurotoxic effects. Moreover, monocytes entering the brain from the periphery during disease course might add to disease pathophysiology...
August 25, 2016: Brain Pathology
https://www.readbyqxmd.com/read/27301858/early-life-stress-perturbs-the-maturation-of-microglia-in-the-developing-hippocampus
#2
Jean-Christophe Delpech, Lan Wei, Jin Hao, Xiaoqing Yu, Charlotte Madore, Oleg Butovsky, Arie Kaffman
Children exposed to abuse or neglect show abnormal hippocampal development and similar findings have been reported in rodent models. Using brief daily separation (BDS), a mouse model of early life stress, we previously showed that exposure to BDS impairs hippocampal function in adulthood and perturbs synaptic maturation, synaptic pruning, axonal growth and myelination in the developing hippocampus. Given that microglia are involved in these developmental processes, we tested whether BDS impairs microglial activity in the hippocampus of 14 (during BDS) and 28-day old mice (one week after BDS)...
October 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/26847266/dark-microglia-a-new-phenotype-predominantly-associated-with-pathological-states
#3
Kanchan Bisht, Kaushik P Sharma, Cynthia Lecours, Maria Gabriela Sánchez, Hassan El Hajj, Giampaolo Milior, Adrián Olmos-Alonso, Diego Gómez-Nicola, Giamal Luheshi, Luc Vallières, Igor Branchi, Laura Maggi, Cristina Limatola, Oleg Butovsky, Marie-Ève Tremblay
The past decade has witnessed a revolution in our understanding of microglia. These immune cells were shown to actively remodel neuronal circuits, leading to propose new pathogenic mechanisms. To study microglial implication in the loss of synapses, the best pathological correlate of cognitive decline across chronic stress, aging, and diseases, we recently conducted ultrastructural analyses. Our work uncovered the existence of a new microglial phenotype that is rarely present under steady state conditions, in hippocampus, cerebral cortex, amygdala, and hypothalamus, but becomes abundant during chronic stress, aging, fractalkine signaling deficiency (CX3 CR1 knockout mice), and Alzheimer's disease pathology (APP-PS1 mice)...
May 2016: Glia
https://www.readbyqxmd.com/read/26531346/identification-of-a-unique-molecular-and-functional-microglia-signature-in-health-and-disease
#4
Oleg Butovsky, Mark P Jedrychowski, Craig S Moore, Ron Cialic, Amanda J Lanser, Galina Gabriely, Thomas Koeglsperger, Ben Dake, Pauline M Wu, Camille E Doykan, Zain Fanek, LiPing Liu, Zhuoxun Chen, Jeffrey D Rothstein, Richard M Ransohoff, Steven P Gygi, Jack P Antel, Howard L Weiner
No abstract text is available yet for this article.
December 2015: International Journal of Developmental Neuroscience
https://www.readbyqxmd.com/read/26531345/targeting-mir-155-restores-dysfunctional-microglia-and-ameliorates-disease-in-the-sod1-model-of-als
#5
Oleg Butovsky, Mark P Jedrychowski, Ron Cialic, Gopal Murugaiyan, Pauline M Wu, Camille E Doykan, Zain Fanek, David J Greco, Olga Kiner, Robert J Lawson, Matthew P Frosch, Nathalie Pochet, Anna M Krichevsky, Steven P Gygi, James Berry, Merit E Cudkowicz, Howard L Weiner
No abstract text is available yet for this article.
December 2015: International Journal of Developmental Neuroscience
https://www.readbyqxmd.com/read/26436904/depletion-of-microglia-and-inhibition-of-exosome-synthesis-halt-tau-propagation
#6
Hirohide Asai, Seiko Ikezu, Satoshi Tsunoda, Maria Medalla, Jennifer Luebke, Tarik Haydar, Benjamin Wolozin, Oleg Butovsky, Sebastian Kügler, Tsuneya Ikezu
Accumulation of pathological tau protein is a major hallmark of Alzheimer's disease. Tau protein spreads from the entorhinal cortex to the hippocampal region early in the disease. Microglia, the primary phagocytes in the brain, are positively correlated with tau pathology, but their involvement in tau propagation is unknown. We developed an adeno-associated virus-based model exhibiting rapid tau propagation from the entorhinal cortex to the dentate gyrus in 4 weeks. We found that depleting microglia dramatically suppressed the propagation of tau and reduced excitability in the dentate gyrus in this mouse model...
November 2015: Nature Neuroscience
https://www.readbyqxmd.com/read/25846981/identification-of-a-chronic-non-neurodegenerative-microglia-activation-state-in-a-mouse-model-of-peroxisomal-%C3%AE-oxidation-deficiency
#7
Simon Verheijden, Lien Beckers, Andrea Casazza, Oleg Butovsky, Massimiliano Mazzone, Myriam Baes
The functional diversity and molecular adaptations of reactive microglia in the chronically inflamed central nervous system (CNS) are poorly understood. We previously showed that mice lacking multifunctional protein 2 (MFP2), a pivotal enzyme in peroxisomal β-oxidation, persistently accumulate reactive myeloid cells in the gray matter of the CNS. Here, we show that the increased numbers of myeloid cells solely derive from the proliferation of resident microglia and not from infiltrating monocytes. We defined the signature of Mfp2(-/-) microglia by gene expression profiling after acute isolation, which was validated by quantitative polymerase reaction (qPCR), immunohistochemical, and flow cytometric analysis...
September 2015: Glia
https://www.readbyqxmd.com/read/25821842/p2y12-expression-and-function-in-alternatively-activated-human-microglia
#8
Craig S Moore, Ariel R Ase, Angham Kinsara, Vijayaraghava T S Rao, Mackenzie Michell-Robinson, Soo Yuen Leong, Oleg Butovsky, Samuel K Ludwin, Philippe Séguéla, Amit Bar-Or, Jack P Antel
OBJECTIVE: To investigate and measure the functional significance of altered P2Y12 expression in the context of human microglia activation. METHODS: We performed in vitro and in situ experiments to measure how P2Y12 expression can influence disease-relevant functional properties of classically activated (M1) and alternatively activated (M2) human microglia in the inflamed brain. RESULTS: We demonstrated that compared to resting and classically activated (M1) human microglia, P2Y12 expression is increased under alternatively activated (M2) conditions...
April 2015: Neurology® Neuroimmunology & Neuroinflammation
https://www.readbyqxmd.com/read/25732305/trem2-deficiency-eliminates-trem2-inflammatory-macrophages-and-ameliorates-pathology-in-alzheimer-s-disease-mouse-models
#9
Taylor R Jay, Crystal M Miller, Paul J Cheng, Leah C Graham, Shane Bemiller, Margaret L Broihier, Guixiang Xu, Daniel Margevicius, J Colleen Karlo, Gregory L Sousa, Anne C Cotleur, Oleg Butovsky, Lynn Bekris, Susan M Staugaitis, James B Leverenz, Sanjay W Pimplikar, Gary E Landreth, Gareth R Howell, Richard M Ransohoff, Bruce T Lamb
Variants in triggering receptor expressed on myeloid cells 2 (TREM2) confer high risk for Alzheimer's disease (AD) and other neurodegenerative diseases. However, the cell types and mechanisms underlying TREM2's involvement in neurodegeneration remain to be established. Here, we report that TREM2 is up-regulated on myeloid cells surrounding amyloid deposits in AD mouse models and human AD tissue. TREM2 was detected on CD45(hi)Ly6C(+) myeloid cells, but not on P2RY12(+) parenchymal microglia. In AD mice deficient for TREM2, the CD45(hi)Ly6C(+) macrophages are virtually eliminated, resulting in reduced inflammation and ameliorated amyloid and tau pathologies...
March 9, 2015: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/25381879/targeting-mir-155-restores-abnormal-microglia-and-attenuates-disease-in-sod1-mice
#10
Oleg Butovsky, Mark P Jedrychowski, Ron Cialic, Susanne Krasemann, Gopal Murugaiyan, Zain Fanek, David J Greco, Pauline M Wu, Camille E Doykan, Olga Kiner, Robert J Lawson, Matthew P Frosch, Nathalie Pochet, Rachid El Fatimy, Anna M Krichevsky, Steven P Gygi, Hans Lassmann, James Berry, Merit E Cudkowicz, Howard L Weiner
OBJECTIVE: To investigate miR-155 in the SOD1 mouse model and human sporadic and familial amyotrophic lateral sclerosis (ALS). METHODS: NanoString microRNA, microglia and immune gene profiles, protein mass spectrometry, and RNA-seq analyses were measured in spinal cord microglia, splenic monocytes, and spinal cord tissue from SOD1 mice and in spinal cord tissue of familial and sporadic ALS. miR-155 was targeted by genetic ablation or by peripheral or centrally administered anti-miR-155 inhibitor in SOD1 mice...
January 2015: Annals of Neurology
https://www.readbyqxmd.com/read/25157514/corrigendum-identification-of-a-unique-tgf-%C3%AE-dependent-molecular-and-functional-signature-in-microglia
#11
Oleg Butovsky, Mark P Jedrychowski, Craig S Moore, Ron Cialic, Amanda J Lanser, Galina Gabriely, Thomas Koeglsperger, Ben Dake, Pauline M Wu, Camille E Doykan, Zain Fanek, LiPing Liu, Zhuoxun Chen, Jeffrey D Rothstein, Richard M Ransohoff, Steven P Gygi, Jack P Antel, Howard L Weiner
No abstract text is available yet for this article.
August 26, 2014: Nature Neuroscience
https://www.readbyqxmd.com/read/25002752/differential-roles-of-microglia-and-monocytes-in-the-inflamed-central-nervous-system
#12
Ryo Yamasaki, Haiyan Lu, Oleg Butovsky, Nobuhiko Ohno, Anna M Rietsch, Ron Cialic, Pauline M Wu, Camille E Doykan, Jessica Lin, Anne C Cotleur, Grahame Kidd, Musab M Zorlu, Nathan Sun, Weiwei Hu, LiPing Liu, Jar-Chi Lee, Sarah E Taylor, Lindsey Uehlein, Debra Dixon, Jinyu Gu, Crina M Floruta, Min Zhu, Israel F Charo, Howard L Weiner, Richard M Ransohoff
In the human disorder multiple sclerosis (MS) and in the model experimental autoimmune encephalomyelitis (EAE), macrophages predominate in demyelinated areas and their numbers correlate to tissue damage. Macrophages may be derived from infiltrating monocytes or resident microglia, yet are indistinguishable by light microscopy and surface phenotype. It is axiomatic that T cell-mediated macrophage activation is critical for inflammatory demyelination in EAE, yet the precise details by which tissue injury takes place remain poorly understood...
July 28, 2014: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/24316888/identification-of-a-unique-tgf-%C3%AE-dependent-molecular-and-functional-signature-in-microglia
#13
Oleg Butovsky, Mark P Jedrychowski, Craig S Moore, Ron Cialic, Amanda J Lanser, Galina Gabriely, Thomas Koeglsperger, Ben Dake, Pauline M Wu, Camille E Doykan, Zain Fanek, Liping Liu, Zhuoxun Chen, Jeffrey D Rothstein, Richard M Ransohoff, Steven P Gygi, Jack P Antel, Howard L Weiner
Microglia are myeloid cells of the CNS that participate both in normal CNS function and in disease. We investigated the molecular signature of microglia and identified 239 genes and 8 microRNAs that were uniquely or highly expressed in microglia versus myeloid and other immune cells. Of the 239 genes, 106 were enriched in microglia as compared with astrocytes, oligodendrocytes and neurons. This microglia signature was not observed in microglial lines or in monocytes recruited to the CNS, and was also observed in human microglia...
January 2014: Nature Neuroscience
https://www.readbyqxmd.com/read/22863620/modulating-inflammatory-monocytes-with-a-unique-microrna-gene-signature-ameliorates-murine-als
#14
Oleg Butovsky, Shafiuddin Siddiqui, Galina Gabriely, Amanda J Lanser, Ben Dake, Gopal Murugaiyan, Camille E Doykan, Pauline M Wu, Reddy R Gali, Lakshmanan K Iyer, Robert Lawson, James Berry, Anna M Krichevsky, Merit E Cudkowicz, Howard L Weiner
Amyotrophic lateral sclerosis (ALS) is a progressive disease associated with neuronal cell death that is thought to involve aberrant immune responses. Here we investigated the role of innate immunity in a mouse model of ALS. We found that inflammatory monocytes were activated and that their progressive recruitment to the spinal cord, but not brain, correlated with neuronal loss. We also found a decrease in resident microglia in the spinal cord with disease progression. Prior to disease onset, splenic Ly6Chi monocytes expressed a polarized macrophage phenotype (M1 signature), which included increased levels of chemokine receptor CCR2...
September 2012: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/22073221/excess-circulating-alternatively-activated-myeloid-m2-cells-accelerate-als-progression-while-inhibiting-experimental-autoimmune-encephalomyelitis
#15
Ilan Vaknin, Gilad Kunis, Omer Miller, Oleg Butovsky, Shay Bukshpan, David R Beers, Jenny S Henkel, Eti Yoles, Stanley H Appel, Michal Schwartz
BACKGROUND: Circulating immune cells including autoreactive T cells and monocytes have been documented as key players in maintaining, protecting and repairing the central nervous system (CNS) in health and disease. Here, we hypothesized that neurodegenerative diseases might be associated, similarly to tumors, with increased levels of circulating peripheral myeloid derived suppressor cells (MDSCs), representing a subset of suppressor cells that often expand under pathological conditions and inhibit possible recruitment of helper T cells needed for fighting off the disease...
2011: PloS One
https://www.readbyqxmd.com/read/21738414/heavy-metals-in-carabids-coleoptera-carabidae
#16
Ruslan O Butovsky
Carabid beetles (Coleoptera, Carabidae) are one of the most studied soil groups in relation to heavy metal (HM) accumulation and use for bioindication of environmental pollution. Accumulation of Zn and Cu in carabid beetles was species-, sex- and trophic group-specific. No differences were found in HM contents between omnivorous and carnivorous species. The use of carabid beetles as indicators of HM accumulation appears to be rather limited.
2011: ZooKeys
https://www.readbyqxmd.com/read/19085384/weekly-vaccination-with-copaxone-glatiramer-acetate-as-a-potential-therapy-for-dry-age-related-macular-degeneration
#17
RANDOMIZED CONTROLLED TRIAL
Gennady Landa, Oleg Butovsky, Johai Shoshani, Michal Schwartz, Ayala Pollack
PURPOSE: Drusen formation in age-related macular degeneration (AMD) shares some similarities with Alzheimer's disease (AD), which is associated with amyloid deposits. Aggregated beta-amyloid induces microglia to become cytotoxic and block neurogenesis. Recent evidence showed that T cell-based vaccination with Copaxone in AD mice model resulted in modulation of microglia into neuroprotective phenotype and as a result in reduction of cognitive decline, elimination of plaque formation, and induction of neuronal survival and neurogenesis...
November 2008: Current Eye Research
https://www.readbyqxmd.com/read/18147951/-survey-of-food-consumption-in-rural-households
#18
B BUTOVSKY
No abstract text is available yet for this article.
July 1949: Výz̆iva Lidu
https://www.readbyqxmd.com/read/18040786/does-inflammation-in-an-autoimmune-disease-differ-from-inflammation-in-neurodegenerative-diseases-possible-implications-for-therapy
#19
REVIEW
Michal Schwartz, Oleg Butovsky, Jonathan Kipnis
Accumulating evidence suggests that neurodegenerative diseases of the central nervous system (CNS) are associated with a local inflammatory response. CNS autoimmune diseases are also associated with inflammation. Does this mean that all neurodegenerative diseases are autoimmune in nature? Does it imply that autoimmune and neurodegenerative diseases are both eligible for the same therapy? What distinguishes between the two types of disease? Do they differ both in etiology and in pathology, or do they have different etiologies but similar pathology and progression? In this minireview we offer a new view of the inflammatory differences between neurodegenerative and autoimmune diseases in the CNS and discuss the implications for therapy...
March 2006: Journal of Neuroimmune Pharmacology: the Official Journal of the Society on NeuroImmune Pharmacology
https://www.readbyqxmd.com/read/17675603/recast-density-and-acquisition-of-novel-irregular-past-tense-verbs
#20
Kerry Proctor-Williams, Marc E Fey
PURPOSE: Children with specific language impairment (SLI) lag behind children with typical language (TL) in their grammatical development, despite equivalent early exposure to recasts in conversation (M. E. Fey, T. E. Krulik, D. F. Loeb, & K. Proctor-Williams, 1999) and the ability to learn from recasts in intervention as quickly as do children with TL (K. E. Nelson, S. Camarata, J. Welsh, L. Butovsky, & M. Camarata, 1996). This experiment tested whether this apparent paradox could be attributed to variations in the density of recasts in conversation versus intervention...
August 2007: Journal of Speech, Language, and Hearing Research: JSLHR
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