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Curr Alzheimer Res. 2020 Feb 12. doi: 10.2174/1567205017666200212155234. [Epub ahead of print]

Microglia in Alzheimer's Disease.

Author information

1
Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Germany.
2
Department of Cellular and Molecular Medicine, University of California, San Diego, 9500, Gilman Drive, La Jolla, CA 92093-0651, United States.

Abstract

Alzheimer's Disease (AD) is the most frequent neurodegenerative disorder. Although proteinaceous aggregates of extracellular amyloid-β (Aβ) and intracellular hyperphosphorylated microtubuleassociated tau have long been identified as characteristic neuropathological hallmarks of AD, a diseasemodifying therapy against these targets has not been successful. An emerging concept is that microglia, the innate immune cells of the brain, are major players in AD pathogenesis. Microglia are long-lived tissue-resident professional phagocytes that survey and rapidly respond to changes in their microenvironment. Subpopulations of microglia cluster around Aβ plaques and adopt a transcriptomic signature specifically linked to neurodegeneration. A plethora of molecules and pathways associated with microglia function and dysfunction has been identified in playing crucial roles in mediating neurodegeneration. However, whether microglia exert either beneficial or detrimental effects in AD pathology may depend on the disease stage. In this review, we summarize the current knowledge about the stage-dependent role of microglia activation in AD, including recent insights from genetic and gene expression profiling studies as well as novel imaging techniques focusing on microglia in human AD pathology and AD mouse models.

KEYWORDS:

Alzheimer's Disease; Genetics; Microglia; Transcriptomics

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