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- J S Malter, B C Ray, P R Westmark, and C J Westmark.
- Department of Pathology, Waisman Center for Developmental Disabilities, UWMadison, WI, USA. jsmalter@wisc.edu
- Curr Alzheimer Res. 2010 May 1; 7 (3): 200-6.
AbstractAs the mechanisms underlying neuronal development and degeneration become clarified, a number of common effectors and signaling pathways are becoming apparent. Here we describe the identification of Abeta, long considered a pathologic mediator of Alzheimers Disease and Down Syndrome, as similarly over-expressed in the neurodevelopmental disease, Fragile X Syndrome. We also show that mGluR5 inhibitors, currently employed for the treatment of Fragile X, reduce Abeta production in rodent models of Fragile X and AD as well as reduce disease phenotypes including seizures. Thus seemingly disparate neurologic diseases may share a common pathologic instigator and be treatable with a common, currently available class of therapeutics.
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