2型糖尿病患病人數(shù)呈現(xiàn)快速增加的趨勢(shì),由其引發(fā)的認(rèn)知功能障礙成為被關(guān)注的熱點(diǎn),但其發(fā)病機(jī)制尚不完全清楚.近年來(lái)一種2型糖尿病的“炎癥學(xué)說(shuō)”逐漸被越來(lái)越多的學(xué)者所提及,并且越來(lái)越多的研究發(fā)現(xiàn)某些因素能夠介導(dǎo)神經(jīng)炎癥從而引發(fā)2型糖尿病腦病,將從小膠質(zhì)細(xì)胞活化、外周細(xì)胞因子、晚期糖基化終產(chǎn)物(AGEs)與β淀粉樣肽(Aβ)等方面對(duì)2型糖尿病腦病的引發(fā)進(jìn)行綜述,為其治療藥物的開(kāi)發(fā)提供參考.

The number of patients with type 2 diabetes mellitus (T2DM) shows a rapid increasing trend, and the cognitive dysfunction which is caused by T2DM has been a hot spot of attention, but its pathogenesis are still not entirely clear. In recent years, “the inflammation hypothesis of T2DM” has been mentioned by many researchers, and more and more researches had found that neuroinflammation could act as a trigger for type 2 diabetic encephalopathy (T2DE) which could be mediated by some factors. This review summarizes the factors which could mediate neuroinflammation causing T2DE, including the activation of microglial cells, periphery cytokines, advanced glycation end products (AGEs), β amyloid peptide, and so on, in order to provide reference for the development of treatment drugs.

國(guó)家自然科學(xué)基金資助項(xiàng)目(81403213)