The X11 proteins, Aβ production and Alzheimer's disease

Cerebral deposition of amyloid-β peptide (Aβ) within neuritic plaques is a hallmark pathology of Alzheimer's disease. It is now generally believed that the development of this pathology is central to the pathogenesis of Alzheimer's disease. As such, inhibiting Aβ deposition or removing Aβ deposits once they are formed represent therapeutic targets for Alzheimer's disease. Aβ is derived from a precursor, the amyloid precursor protein (APP), and APP binds to the X11 family of adaptor proteins. Studies from several laboratories have now shown that X11α and X11β (the two neuronal X11s) inhibit APP processing and Aβ production. Exactly how this is achieved is not yet known but recent studies in which other X11 binding partners have been identified are beginning to reveal potential mechanisms.