期刊
TRENDS IN MOLECULAR MEDICINE
卷 14, 期 2, 页码 45-53出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2007.12.002
关键词
-
资金
- NIA NIH HHS [R01 AG028072-02, R01 AG028072, AG026051, AG028072] Funding Source: Medline
Recent studies of postmortem brains from Alzheimer's disease (AD) patients and transgenic mouse models of AD suggest that oxidative damage, induced by amyloid beta (A beta), is associated with mitochondria early in AD progression. A beta and amyloid-precursor protein are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron-transport chain, increase reactive oxygen species production, cause mitochondrial damage and prevent neurons from functioning normally. Furthermore, accumulation of A beta at synaptic terminals might contribute to synaptic damage and cognitive decline in patients with AD. Here, we describe recent studies regarding the roles of A beta and mitochondrial function in AD progression and particularly in synaptic damage and cognitive decline.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据