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Antioxid Redox Signal. 2012 Jun 15;16(12):1434-55. doi: 10.1089/ars.2011.4149. Epub 2011 Sep 15.

Mitochondria and cell bioenergetics: increasingly recognized components and a possible etiologic cause of Alzheimer's disease.

Author information

1
Department of Neurology, University of Kansas Medical Center, Kansas City, Kansas, USA. rswerdlow@kumc.edu

Abstract

SIGNIFICANCE:

Mitochondria and brain bioenergetics are increasingly thought to play an important role in Alzheimer's disease (AD).

RECENT ADVANCES:

Data that support this view are discussed from the perspective of the amyloid cascade hypothesis, which assumes beta-amyloid perturbs mitochondrial function, and from an opposite perspective that assumes mitochondrial dysfunction promotes brain amyloidosis. A detailed review of cytoplasmic hybrid (cybrid) studies, which argue mitochondrial DNA (mtDNA) contributes to sporadic AD, is provided. Recent AD endophenotype data that further suggest an mtDNA contribution are also summarized.

CRITICAL ISSUES AND FUTURE DIRECTIONS:

Biochemical, molecular, cybrid, biomarker, and clinical data pertinent to the mitochondria-bioenergetics-AD nexus are synthesized and the mitochondrial cascade hypothesis, which represents a mitochondria-centric attempt to conceptualize sporadic AD, is discussed.

PMID:
21902597
PMCID:
PMC3329949
DOI:
10.1089/ars.2011.4149
[Indexed for MEDLINE]
Free PMC Article

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