期刊
JOURNAL OF MOLECULAR NEUROSCIENCE
卷 62, 期 2, 页码 215-221出版社
HUMANA PRESS INC
DOI: 10.1007/s12031-017-0928-7
关键词
Load; Case-control study; Microglial genes; Polymorphisms
资金
- Nucleo de Genetica Humana e Molecular - NGHM, Brazil
- Universidade Federal do Espirito Santo - UFES
- Fundo de Amparo e Pesquisa do Espirito Santo - FAPES
- Departamento de Ciencia e Tecnologia do Ministerio da Saude - Decit
- Secretaria de Ciencia, Tecnologia e Insumos Estrategicos do Ministerio da Saude - SCTIE/MS
- Fundo de Apoio a Ciencia e Tecnologia do Municipio de Vitoria - FACITEC
- Ministerio da Ciencia, Tecnologia e Inovacao - MCTI
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - CNPQ
- Ministerio da Educacao - MEC
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - CAPES
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 A beta 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 A beta 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.
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