Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Brain Res Brain Res Rev. 2005 Nov;49(3):618-32. Epub 2005 Apr 19.

Are mitochondria critical in the pathogenesis of Alzheimer's disease?

Author information

  • 1Neurogenetics Laboratory, Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA. reddyh@ohsu.edu

Abstract

This review summarizes recent findings that suggest a causal connection between mitochondrial abnormalities and sporadic Alzheimer's disease (AD). Genetic causes of AD are known only for a small proportion of familial AD patients, but for a majority of sporadic AD patients, genetic causal factors are still unknown. Currently, there are no early detectable biomarkers for sporadic AD, and there is a lack of understanding of the pathophysiology of the disease. Findings from recent genetic studies of AD pathogenesis suggest that mitochondrial defects may play an important role in sporadic AD progression, and that mitochondrial abnormalities and oxidative damage may play a significant role in the progression of familial AD. Findings from biochemical studies, in vitro studies, gene expression studies, and animal model studies of AD are reviewed, and the possible contribution of mitochondrial mutations to late-onset sporadic AD is discussed.

PMID:
16269322
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk