| Literature DB >> 28477215 |
Lígia Ramos Dos Santos1,2, Lúcia Helena Sagrillo Pimassoni3, Geralda Gillian Silva Sena4,5, Daniela Camporez4,6, Luciano Belcavello4, Maíra Trancozo4,6, Renato Lírio Morelato3,7, Flavia Imbroisi Valle Errera6,3, Maria Rita Passos Bueno8, Flavia de Paula4,6.
Abstract
Late-onset Alzheimer's disease (LOAD) is a multifactorial neurodegenerative disorder that corresponds to most Alzheimer's disease (AD) cases. Inflammation is frequently related to AD, whereas microglial cells are the major phagocytes in the brain and mediate the removal of Aβ peptides. Microglial cell dsyregulation might contribute to the formation of amyloid plaques, a hallmark of AD. Genome-wide association studies have reported genetic loci associated with the inflammatory pathway involved in AD. Among them, rs3865444 CD33, rs3764650 ABCA7, rs6656401 CR1, and rs610932 MS4A6A variants in microglial genes are associated with LOAD. These variants are proposed to participate in the clearance of Aβ peptides. However, their association with LOAD was not validated in all case-control studies. Thus, the present work aimed to assess the involvement of CD33 (rs3865444), ABCA7 (rs3764650), CR1 (rs6656401), and MS4A6A (rs610932) with LOAD in a sample from southeastern Brazil. The genotype frequencies were assessed in 79 AD patients and 145 healthy elders matched for sex and age. We found that rs3865444 CD33 acts as a protective factor against LOAD. These results support a role for the inflammatory pathway in LOAD.Entities:
Keywords: Case-control study; Load; Microglial genes; Polymorphisms
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Year: 2017 PMID： 28477215 DOI： 10.1007/s12031-017-0928-7
Source DB: PubMed Journal: J Mol Neurosci ISSN： 0895-8696 Impact factor: 3.444