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Alzheimer's research team employs stem cells to understand disease processes and study new treatment
Date:3/6/2014

cellular location, amyloid-beta protein generation, and then alters Tau protein expression and phosphorylation which impacts the Tau protein's function and activity. Next, the researchers tested multiple amyloid-beta antibodies on the affected neurons. Here, they demonstrated that the secondary increase in Tau can be rescued by treatment with the amyloid -protein antibodies, providing direct evidence linking disease-relevant changes in amyloid-beta to aberrant Tau metabolism in living cells obtained directly from an AD patient.

While AD is characterized by the presence of amyloid-beta protein plaques and Tau protein tangles, observing living cell behavior and understanding the mechanisms and relationship between these abnormal protein deposits and tangles has been challenging. Experimental treatments for AD are using antibodies to try to neutralize the toxic effects of amyloid-beta, because they can bind to and clear the amyoid-beta peptide from the brain.

This study is the first of its kind to examine the effects of antibody therapy on human neurons derived directly from patients with familial AD.

"Amyloid-beta immunotherapy is a promising therapeutic option in AD, if delivered early in the disease process," said Dr. Young-Pearse. "Our study suggests that this stem cell model from actual patients may be useful in testing and comparing amyloid-beta antibodies, as well as other emerging therapeutic strategies in treating AD."


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Contact: Jessica Maki
jmaki3@partners.org
617-525-6373
Brigham and Women's Hospital
Source:Eurekalert

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