JOURNAL ARTICLE
Alzheimer's Disease Genetics: A Dampened Microglial Response?
Published In: Neuroscientist, 2023, v. 29, n. 2. P. 245 1 of 3
Database: Academic Search Ultimate 2 of 3
Authored By: Chatila, Zena K.; Bradshaw, Elizabeth M. 3 of 3
Abstract
The article focuses on the role of microglia, the central nervous system's resident innate immune cells, in the pathogenesis of late-onset Alzheimer's disease (LOAD), emphasizing insights gained from genetic studies. It highlights that many genetic risk variants associated with LOAD converge to suppress activating microglial receptors and enhance inhibitory receptor function, resulting in a dampened microglial phenotype that may impair clearance of amyloid-beta and resolution of inflammation. Key genes discussed include CD33, TREM2, PILRA, SPI1 (encoding the transcription factor PU.1), PLCG2, IL34, and HLA loci, which interact within shared signaling pathways influencing microglial activation and immune responses. The article also considers the potential interplay between microglial dysfunction, aging-related immunosenescence, and infectious agents in disease progression, suggesting that therapeutic strategies targeting microglial pathways could be promising for LOAD intervention.
Additional Information
- Source:Neuroscientist. 2023/04, Vol. 29, Issue 2, p245
- Document Type:Article
- Subject Area:Health and Medicine
- Publication Date:2023
- ISSN:1073-8584
- DOI:10.1177/10738584211024531
- Accession Number:162431627
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