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Curr Alzheimer Res. 2010 May;7(3):200-6.

Fragile X Syndrome and Alzheimer's Disease: Another story about APP and beta-amyloid.

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  • 1Department of Pathology, Waisman Center for Developmental Disabilities, UWMadison, WI, USA. jsmalter@wisc.edu

Abstract

As 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.

PMID:
20088809
[PubMed - indexed for MEDLINE]
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