Journal
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
Volume 35, Issue 2, Pages 320-330Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pnpbp.2010.07.004
Keywords
Alzheimer's disease; APOE4; Mitochondrial DNA (mtDNA); Mitochondrial dysfunction; Mitochondrial haplogroups; Oxidative stress
Funding
- Ministry of Science and Higher Education (MNiSzW) [NN 401 0622 35, PBZ-MEiN 9/2/20/17]
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To date, one of the most discussed hypotheses for Alzheimer's disease (AD) etiology implicates mitochondrial dysfunction and oxidative stress as one of the primary events in the course of AD. In this review we focus on the role of mitochondria and mitochondrial DNA (mtDNA) variation in AD and discuss the rationale for the involvement of mitochondrial abnormalities in AD pathology. We summarize the current data regarding the proteins involved in mitochondrial function and pathology observed in AD, and discuss the role of somatic mutations and mitochondrial haplogroups in AD development. (C) 2010 Elsevier Inc. All rights reserved.
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