Microglia and Neuroinflammation: What Place for P2RY12? DOI Open Access
Albert Gómez Morillas, Valérie C. Besson, Dominique Lerouet

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(4), P. 1636 - 1636

Published: Feb. 6, 2021

Microglia are immune brain cells involved in neuroinflammation. They express a lot of proteins on their surface such as receptors that can be activated by mediators released the microglial environment. Among these receptors, purinergic receptor expression could modified depending activation status microglia. In this review, we focus P2Y and more specifically P2RY12 is motility migration, first step neuroinflammation process. We describe families, structure, physiological functions. The pharmacological genetic tools for studying detailed thereafter. Last but not least, report contribution to acute chronic pathologies order better understand role.

Language: Английский

How microglia sense and regulate neuronal activity DOI
Anthony D. Umpierre, Long‐Jun Wu

Glia, Journal Year: 2020, Volume and Issue: 69(7), P. 1637 - 1653

Published: Dec. 28, 2020

Microglia are innate immune cells of the central nervous system that sense extracellular cues. Brain injuries, inflammation, and pathology evoke dynamic structural responses in microglia, altering their morphology motility. The motility microglia is hypothesized to be a critical first step sensing local alterations engaging pattern-specific responses. Alongside pathological responses, also regulate neuronal activity. In this review, we consider molecules, receptors, mechanisms allow activity changes under both hypoactivity hyperactivity. We highlight emerging vivo evidence activity, ranging from physiological pathophysiological conditions. addition, discuss role calcium signaling microglial environment. function monitoring influencing may for brain homeostasis circuit modification health disease.

Language: Английский

Citations

150

Perivascular cells induce microglial phagocytic states and synaptic engulfment via SPP1 in mouse models of Alzheimer’s disease DOI Creative Commons
Sebastiaan De Schepper,

Judy Z. Ge,

Gerard Crowley

et al.

Nature Neuroscience, Journal Year: 2023, Volume and Issue: 26(3), P. 406 - 415

Published: Feb. 6, 2023

Alzheimer's disease (AD) is characterized by synaptic loss, which can result from dysfunctional microglial phagocytosis and complement activation. However, what signals drive aberrant microglia-mediated engulfment of synapses in AD unclear. Here we report that secreted phosphoprotein 1 (SPP1/osteopontin) upregulated predominantly perivascular macrophages and, to a lesser extent, fibroblasts. Perivascular SPP1 required for microglia engulf upregulate phagocytic markers including C1qa, Grn Ctsb presence amyloid-β oligomers. Absence Spp1 expression mouse models results prevention loss. Furthermore, single-cell RNA sequencing putative cell-cell interaction analyses reveal induces states the hippocampus model AD. Altogether, suggest functional role cells-to-microglia crosstalk, whereby modulates

Language: Английский

Citations

150

Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity DOI Creative Commons
Matheus B. Victor,

Noelle Leary,

Xochitl Luna

et al.

Cell stem cell, Journal Year: 2022, Volume and Issue: 29(8), P. 1197 - 1212.e8

Published: Aug. 1, 2022

Language: Английский

Citations

148

Microglia and Neuroinflammation: Crucial Pathological Mechanisms in Traumatic Brain Injury-Induced Neurodegeneration DOI Creative Commons

Fangjie Shao,

Xiaoyu Wang, Haijian Wu

et al.

Frontiers in Aging Neuroscience, Journal Year: 2022, Volume and Issue: 14

Published: March 25, 2022

Traumatic brain injury (TBI) is one of the most common diseases in central nervous system (CNS) with high mortality and morbidity. Patients TBI usually suffer many sequelae life time post injury, including neurodegenerative disorders such as Alzheimer’s disease (AD) Parkinson’s (PD). However, pathological mechanisms connecting these two processes have not yet been fully elucidated. It important to further investigate pathophysiological underlying TBI-induced neurodegeneration, which will promote development precise treatment target for notorious consequences after TBI. A growing body evidence shows that neuroinflammation a pivotal process chronic neurodegeneration following Microglia, immune cells CNS, play crucial roles other CNS diseases. Of interest, microglial activation functional alteration has proposed key mediators evolution pathology Here, we review updated studies involving phenotypical alterations microglia survey molecules regulating activities responses pathology, explore their potential implications injury. The work give us comprehensive understanding driving TBI-related offer novel ideas developing corresponding prevention strategies this disease.

Language: Английский

Citations

141

Microglia and Neuroinflammation: What Place for P2RY12? DOI Open Access
Albert Gómez Morillas, Valérie C. Besson, Dominique Lerouet

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(4), P. 1636 - 1636

Published: Feb. 6, 2021

Microglia are immune brain cells involved in neuroinflammation. They express a lot of proteins on their surface such as receptors that can be activated by mediators released the microglial environment. Among these receptors, purinergic receptor expression could modified depending activation status microglia. In this review, we focus P2Y and more specifically P2RY12 is motility migration, first step neuroinflammation process. We describe families, structure, physiological functions. The pharmacological genetic tools for studying detailed thereafter. Last but not least, report contribution to acute chronic pathologies order better understand role.

Language: Английский

Citations

134