TY - JOUR
T1 - Are mitochondria critical in the pathogenesis of Alzheimer's disease?
AU - Reddy, P. Hemachandra
AU - Beal, M. Flint
N1 - Funding Information:
The authors thank Sandra Oster, Neurological Sciences Institute, Oregon Health and Science University, for critical reading of the review. This research was supported, in part, by the American Federation for Aging Research and NIH #AG22643.
PY - 2005/11
Y1 - 2005/11
N2 - 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.
AB - 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.
KW - In vitro studies
KW - Mitochondria
KW - Mitochondrial gene expression
KW - Mitochondrial mutations
KW - Oxidative damage
KW - Peripheral cells
KW - Sporadic Alzheimer's disease
KW - Transgenic mice
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U2 - 10.1016/j.brainresrev.2005.03.004
DO - 10.1016/j.brainresrev.2005.03.004
M3 - Review article
C2 - 16269322
AN - SCOPUS:27544484846
SN - 0165-0173
VL - 49
SP - 618
EP - 632
JO - Brain Research Reviews
JF - Brain Research Reviews
IS - 3
ER -