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 epsilon4 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 beta-amyloid peptide (Abeta) 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.
炎症反应在阿尔茨海默病的进展中发挥着重要的作用。 近来流行病学研究显示炎症介质的基因多态性可以影响阿尔茨海默病在人群中的发病率。 另有报道, ApoE ɛ4, 阿尔茨海默病的危险因子, 可直接增强炎症反应。 因此, 在老龄化过程中, 个体是否容易罹患阿尔茨海默病, 可能与对Aβ斑块和其他免疫原的长期刺激引发的炎症反应强度有关, 其反应强度取决于其遗传基因。 炎症相关的基因可能影响个体对阿尔茨海默病的易感性, 并可能为将来的阿尔茨海默病危险人群的筛选和个体化治疗提供新的研究方向。