Fragile x Syndrome and Alzheimer's disease: Another story about APP and β-Amyloid

J. S. Malter, B. C. Ray, P. R. Westmark, C. J. Westmark

Research output: Contribution to journalArticle

28 Scopus citations

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 Aβ, 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 Aβ 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.

Original languageEnglish (US)
Pages (from-to)200-206
Number of pages7
JournalCurrent Alzheimer research
Volume7
Issue number3
DOIs
StatePublished - May 1 2010

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Keywords

  • Amyloid precursor protein (APP) and beta-amyloid
  • Fragile x syndrome (FXS)
  • Metabotropic glutamate receptors (mGluR)

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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