Journal
BRAIN RESEARCH
Volume 1415, Issue -, Pages 136-148Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2011.07.052
Keywords
Alzheimer's disease; Mitochondrial dysfunction; Oxidative stress; Hyperphosphorylation of tau; Triple transgenic mice; Amyloid beta; Axonal transport of mitochondria
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Funding
- NIH [AG028072, RR00163]
- Alzheimer Association [IIRG-09-92429]
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Growing evidence suggests that amyloid beta (A beta) and tau pathologies are strongly associated with mitochondrial dysfunction and neuronal damage in Alzheimer's disease (AD). Extensive research of AD postmortem brains, mouse and fly models, including triple transgenic AD mice and mutant tau mice, and cell culture studies revealed that tau hyperphosphorylation is caused by multiple factors, including intraneuronal A beta-oligomers, chronic oxidative stress, reduced insulin-like growth factor 1, and astrocytic mediated-A beta and caspase activation. Overexpressed and phosphorylated tau appears to impair axonal transport of organelles causing synapse starvation, depletion of ATP, and ultimately neuronal damage. This article evaluates the role of tau in mitochondrial dysfunction and assesses how hyperphosphorylated tau impairs axonal transport of organelles in AD neurons. (C) 2011 Elsevier B.V. All rights reserved.
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