Abstract
Microglia, the brain's resident immune cells, are phagocytes of the macrophage lineage that have a key role in responding to inflammation and immune challenge in the brain. More recently, they have been shown to have a number of important roles beyond immune surveillance and response, including synaptic pruning during development and the support of adult neurogenesis. Microglial abnormalities have been found in several neuropsychiatric conditions, though in most cases it remains unclear whether these are causative or are a reaction to some other underlying pathophysiology. Here we summarize postmortem, animal, neuroimaging, and other evidence for microglial pathology in major depression, schizophrenia, autism, obsessive-compulsive disorder, and Tourette syndrome. We identify gaps in the existing literature and important areas for future research. If microglial pathology proves to be an important causative factor in these or other neuropsychiatric diseases, modulators of microglial function may represent a novel therapeutic strategy.
Highlights
Microglia are the brain’s resident immune cells
Unlike neurons and other types of glia, which are of neuroectodermal origin, microglia are macrophage-lineage cells derived from hematopoietic progenitors
Microglia have been presumed to be quiescent under physiological conditions and activated only upon immune challenge or in response to neuronal damage or debris. This is consistent with a role in neurodegeneration, in which microglial activation could be a consequence of a degenerative process, as these phagocytic cells participate in cleaning up cellular debris
Summary
Microglia are the brain’s resident immune cells. Unlike neurons and other types of glia, which are of neuroectodermal origin, microglia are macrophage-lineage cells derived from hematopoietic progenitors. Microglia have been presumed to be quiescent under physiological conditions and activated only upon immune challenge or in response to neuronal damage or debris This is consistent with a role in neurodegeneration, in which microglial activation could be a consequence of a degenerative process, as these phagocytic cells participate in cleaning up cellular debris. They regulate adult neurogenesis [4] This new appreciation that microglia regulate neuronal function and homeostasis under physiological conditions, in the absence of immune challenge or inflammation, raises the possibility that disruption of such processes may contribute to pathological conditions characterized by neuronal or synaptic dysfunction, rather than frank neurodegeneration. Experimental studies recapitulating pathophysiological processes in animal models provide the best avenue to explore this challenging question of causality Such investigations are in their infancy, and a pathogenic role for dysregulated microglia in any neuropsychiatric condition remains largely hypothetical. This is an exciting area of ongoing research in neuropsychiatry
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