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Mol Neurodegener. 2017 May 26;12(1):43. doi: 10.1186/s13024-017-0184-x.

Late onset Alzheimer's disease genetics implicates microglial pathways in disease risk.

Author information

1
Department of Neuroscience, Ronald M. Loeb Center for Alzheimer's disease, Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, New York, NY, 10029, USA.
2
Department of Neuroscience, Ronald M. Loeb Center for Alzheimer's disease, Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, New York, NY, 10029, USA. alison.goate@mssm.edu.

Abstract

Alzheimer's disease (AD) is a highly heritable complex disease with no current effective prevention or treatment. The majority of drugs developed for AD focus on the amyloid cascade hypothesis, which implicates Aß plaques as a causal factor in the disease. However, it is possible that other underexplored disease-associated pathways may be more fruitful targets for drug development. Findings from gene network analyses implicate immune networks as being enriched in AD; many of the genes in these networks fall within genomic regions that contain common and rare variants that are associated with increased risk of developing AD. Of these genes, several (including CR1, SPI1, the MS4As, TREM2, ABCA7, CD33, and INPP5D) are expressed by microglia, the resident immune cells of the brain. We summarize the gene network and genetics findings that implicate that these microglial genes are involved in AD, as well as several studies that have looked at the expression and function of these genes in microglia and in the context of AD. We propose that these genes are contributing to AD in a non-Aß-dependent fashion.

KEYWORDS:

Alzheimer’s disease; Genetics; Microglia; Myeloid

PMID:
28549481
PMCID:
PMC5446752
DOI:
10.1186/s13024-017-0184-x
[Indexed for MEDLINE]
Free PMC Article

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