摘要
微循环障碍是导致肌体局部组织或脏器功能降低的重要原因之一,与衰老、退行性变、免疫功能紊乱等多种疾病的发生发展密切相关.阿尔茨海默病患者中枢神经系统的能量代谢失调、缺血缺氧、代谢产物积累等均累及微循环.本文就甲醛和核糖代谢失调导致的微循环障碍与阿尔茨海默病的典型病理改变(Tau蛋白过度磷酸化、β淀粉样蛋白沉积及认知损伤)之间的关系进行了讨论.
Microcirculation dysfunction is regarded as one of important pathologies of senility, degeneration, immune disorder and many other diseases. Cerebral circulation insufficiency, energetic dysmetabolism, hypoxia-ischemia and metabolites accumulation in Alzheimer's disease (AD) have a close relation with microcirculation dysfunction. Here, we review microcirculation dysfunction playing an important role in hyperphosphorylation of Tau, Aβ aggregation and cognitive impairment induced by accumulation of formaldehyde and D-ribose.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2015年第12期1077-1083,共7页
Progress In Biochemistry and Biophysics
基金
国家重点基础研究发展计划(973)(2012CB911000)
国家自然科学基金(31270868)
中国科学院重点部署项目(20140909)资助~~
关键词
微循环障碍
阿尔茨海默症
内源甲醛
内源核糖
microcirculation dysfunction, Alzheimer's disease (AD), endogenous formaldehyde, endogenous D-ribose