Tuesday, February 09, 2010
   
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Research from University of California, Department of Neurosciences provides new data about Alzheimer disease

Researchers detail in 'Role of synucleins in Alzheimer's disease,' new data in Alzheimer disease. According to recent research published in the journal Neurotoxicity Research, "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 (Abeta) 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 Abeta 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 Abeta 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. Abeta 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 Abeta and alpha-syn might also result in oxidative stress, lysosomal leakage, and mitochondrial dysfunction," wrote L. Crews and colleagues, University of California, Department of Neurosciences (see also Alzheimer Disease).

The researchers concluded: "Thus, better understanding the steps involved in the process of Abeta and alpha-syn aggregation is important in order to develop intervention strategies that might prevent or reverse the accumulation of toxic proteins in AD."

Crews and colleagues published their study in Neurotoxicity Research (Role of synucleins in Alzheimer's disease. Neurotoxicity Research, 2009;16(3):306-17).

For additional information, contact L. Crews, University of California San Diego, Dept. of Neurosciences, La Jolla, CA 92093-0624 USA..

The publisher's contact information for the journal Neurotoxicity Research is: Taylor & Francis Group Ltd, 2 Park Square, Milton Park, Abingdon, Oxford OX14 4RN United Kingdom.



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