Journal
NEUROTOXICITY RESEARCH
Volume 16, Issue 3, Pages 306-317Publisher
SPRINGER
DOI: 10.1007/s12640-009-9073-6
Keywords
Synuclein; Alzheimer's; Parkinson's; Amyloid; APP
Categories
Funding
- NIH [AG18440, AG022074, AG10435, HL066012]
- DOE INCITE
- IBM
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL066012] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG018440, P01AG010435, R37AG018440, P01AG022074] Funding Source: NIH RePORTER
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Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common causes of dementia and movement disorders in the elderly. While progressive accumulation of oligomeric amyloid-beta protein (A beta) has been identified as one of the central toxic events in AD leading to synaptic dysfunction, accumulation of alpha-synuclein (alpha-syn) resulting in the formation of oligomers has been linked to PD. Most of the studies in AD have been focused on investigating the role of A beta and Tau; however, recent studies suggest that alpha-syn might also play a role in the pathogenesis of AD. For example, fragments of alpha-syn can associate with amyloid plaques and A beta promotes the aggregation of alpha-syn in vivo and worsens the deficits in alpha-syn tg mice. Moreover, alpha-syn has also been shown to accumulate in limbic regions in AD, Down's syndrome, and familial AD cases. A beta and alpha-syn might directly interact under pathological conditions leading to the formation of toxic oligomers and nanopores that increase intracellular calcium. The interactions between A beta and alpha-syn might also result in oxidative stress, lysosomal leakage, and mitochondrial dysfunction. Thus, better understanding the steps involved in the process of A beta and alpha-syn aggregation is important in order to develop intervention strategies that might prevent or reverse the accumulation of toxic proteins in AD.
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