Journal
TRENDS IN MOLECULAR MEDICINE
Volume 14, Issue 2, Pages 45-53Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2007.12.002
Keywords
-
Funding
- NIA NIH HHS [R01 AG028072-02, R01 AG028072, AG026051, AG028072] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available