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Obtaining Human Microglia from Adult Human Brain Tissue
Published on: August 30, 2020
The evolving biology of microglia in Alzheimer's disease
Tarja M Malm1, Taylor R Jay, Gary E Landreth
1A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland, tarja.malm@uef.fi.
Abstract:
Alzheimer's disease (AD) is typified by a robust microglial-mediated inflammatory response within the brain. Indeed, microglial accumulation around plaques in AD is one of the classical hallmarks of the disease pathology. Although microglia have the capacity to remove β-amyloid deposits and alleviate disease pathology, they fail to do so. Instead, they become chronically activated and promote inflammation-mediated impairment of cognition and cytotoxicity. However, if microglial function could be altered to engage their phagocytic response, promote their tissue maintenance functions, and prevent release of factors that promote tissue damage, this could provide therapeutic benefit. This review is focused on the current knowledge of microglial homeostatic mechanisms in AD, and mechanisms involved in the regulation of microglial phenotype in this context.
Insights
Alzheimer's disease (AD) involves chronic microglial inflammation that impairs cognition. Modulating microglial function to enhance their protective roles offers potential therapeutic benefits for AD.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Alzheimer's disease (AD) is characterized by significant microglial activation and neuroinflammation.
- Microglia, the brain's immune cells, accumulate around amyloid plaques in AD pathology.
- Despite their potential to clear amyloid, microglia in AD become dysfunctional, promoting cognitive decline and neurotoxicity.
Purpose of the Study:
- To review current knowledge on microglial homeostatic mechanisms in Alzheimer's disease.
- To explore mechanisms regulating microglial phenotype in the context of AD.
- To identify therapeutic strategies targeting microglial dysfunction in AD.
Main Methods:
- Literature review of studies on microglial biology in Alzheimer's disease.
- Analysis of research on microglial activation states and their functional consequences.
- Synthesis of information on factors influencing microglial phenotype and homeostatic functions.
Main Results:
- Microglia in AD exhibit a pro-inflammatory phenotype, contributing to disease progression.
- Dysfunctional microglial phagocytosis fails to clear amyloid-beta plaques effectively.
- Chronic microglial activation leads to impaired cognition and neuronal damage.
Conclusions:
- Altering microglial function to restore homeostatic and phagocytic capabilities is a promising therapeutic avenue for AD.
- Targeting the regulation of microglial phenotype could mitigate neuroinflammation and neurotoxicity in AD.
- Further research into microglial mechanisms is crucial for developing effective Alzheimer's disease treatments.
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