Tuesday, November 27, 2012

Deciphering the mechanism underlying late-onset Alzheimer disease

Drug development efforts for late-onset Alzheimer disease (AD) have met with disappointing results. Krstic and Knuesel argue for a re-evaluation of pathological mechanisms underlying the disease, with a shift of focus away from amyloid-β as the key therapeutic target. Through integration of their own research with the wider literature, they present a model that places inflammation and impairments in axonal functions and integrity at the heart of AD pathology.
Dimitrije Krstic & Irene Knuesel
Nature Reviews Neurology 9, 25-34 (January 2013) | doi:10.1038/nrneurol.2012.236


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