遗传基因的趋炎症性: 阿尔茨海默病的又一危险因素

Abstract

Abstract:Inflammation has been shown to play an important role in the progression of Alzheimer's disease (AD). Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by the gene polymorphisms of the inflammation mediators. Meanwhile, an ensured risk factor, the ApoE ε4 allele is also reported to directly promote inflammation. Accordingly, it appears that an individual genetic background has partly determined his predisposition for AD by the extent of the inflammation response to the chronic stimulus by β-amyloid peptide (Aβ) deposits and other antigen stressor in the elderly. Hence we present a hypothesis that the inflammation genotypes may contribute to AD susceptibility. This may provide a new orientation both for future identification of individuals at risk and for personalized medication.

Tetrahydroxy stilbene glucoside reduces the cognitive impairment and overexpression of amyloid precursor protein induced by aluminum exposure

“…APP expression and processing in the brain is a critical event in the development of AD [23,24] . Here, chronic exposure to Al reduced the latency of avoidance response and increased the expression of APP.…”

Cytokine Gene Polymorphisms and Alzheimer's Disease in Brazil

“…The hazardous effect of a pro-inflammatory profile in AD is supported by epidemiological evidence of a potential protective effect of anti-inflammatory responses [6,7]. In addition, evidence suggests that the risk of AD is affected by genetic variation in inflammatory modulators, such as interleukin 1-alpha ( IL1 -α), IL1-β , IL6 , tumor necrosis factor ( TNF ), and others [8,9]. A recent genome-wide association study has described an association between AD risk and the polymorphic site (rs3818361) at the complement receptor 1 (CR1) gene, placing an immunological marker in the framework of the etiology of AD by indicating unsuitable immune pathways for Aβ clearance as a risk-modifying factor to the progress of the late-onset forms of the disease [10,11].…”

The Gab2 in signal transduction and its potential role in the pathogenesis of Alzheimer’s disease

“…It is characterized by intracellular neurofibrillary tangles (NFTs) containing hyperphosphorylated tau protein, extracellular amyloid plaques containing deposits of beta amyloid (Aβ), and neuronal loss. In recent years, accumulating evidence has indicated that the incidence of AD in some populations is substantially influenced by genetic risk factor [22] . The role of Gab2 in the pathogenesis of AD via tight association with tau and APP has been reported ( Fig.…”