Beta Amyloid Peptide: Research Paper : Microglial Phagocytosis: A Disease-Associated Process Emerging from Alzheimer's Disease Genetics

Microglial Phagocytosis: A Disease-Associated Process Emerging from Alzheimer's Disease Genetics

Abstract

Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease. Genetic studies involving genome-wide association studies (GWAS) and meta-analysis have discovered numerous genomic loci associated with AD; however, the causal genes and variants remain unidentified in most loci. Integration of GWAS signals with epigenomic annotations has demonstrated that AD risk variants are enriched in myeloid-specific enhancers, implicating myeloid cells in AD etiology. AD risk variants in these regulatory elements modify disease susceptibility by regulating the expression of genes that play crucial roles in microglial phagocytosis. Several of these AD risk genes are specifically expressed in myeloid cells, whereas others are ubiquitously expressed but are regulated by AD risk variants within myeloid enhancers in a cell type-specific manner. We discuss the impact of established AD risk variants on microglial phagocytosis and debris processing via the endolysosomal system.

Keywords: Alzheimer's disease; GWAS; endolysosomal network; microglia; phagocytosis.

Copyright © 2020 Elsevier Ltd. All rights reserved.

This article originally appeared in the "https://pubmed.ncbi.nlm.nih.gov/33127097/" and has their copyrights. We do not claim copyright on the content. This information is for research purposes only. This Blog is made available by publishers for educational purposes only as well as to give you general information and a general understanding , not to provide specific advice. By using this blog site you understand that there is no client relationship between you and the Blog publisher. The Blog should not be used as a substitute for competent research advice.