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Mitochondrial Aβ A potential cause of metabolic dysfunction in Alzheimer's disease
Author(s) -
Chen Xi,
Yan Shi Du
Publication year - 2006
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540601047767
Subject(s) - mitochondrion , mitochondrial respiratory chain , alzheimer's disease , neurodegeneration , oxidative stress , respiratory chain , reactive oxygen species , amyloid beta , biology , microbiology and biotechnology , amyloid precursor protein , biochemistry , disease , medicine , peptide
Deficits in mitochondrial function are a characteristic finding in Alzheimer's disease (AD), though the mechanism remains to be clarified. Recent studies revealed that amyloid β peptide (Aβ) gains access into mitochondrial matrix, which was much more pronounced in both AD brain and transgenic mutant APP mice than in normal controls. Aβ progressively accumulates in mitochondria and mediates mitochondrial toxicity. Interaction of mitochondrial Aβ with mitochondrial enzymes such as amyloid β binding alcohol dehydrogenase (ABAD) exaggerates mitochondrial stress by inhibiting the enzyme activity, releasing reactive oxygen species (ROS), and affecting glycolytic, Krebs cycle and/or the respiratory chain pathways through the accumulation of deleterious intermediate metabolites. The pathways proposed may play a key role in the pathogenesis of this devastating neurodegenerative disorder, Alzheimer's disease.iubmb Life, 58: 686‐694, 2006