Newswise — LEXINGTON, Ky. (Jan. 24, 2018) – In an editorial in the most recent edition of the New England Journal of Medicine, a veteran scientist lamented that "we may very well be nearing the end of the amyloid-hypothesis rope" after yet another failed clinical trial for an Alzheimer's drug.

Dr. Michael Murphy, a faculty member at the Sanders-Brown Center on Aging at the University of Kentucky, said that "although it may not quite be time to give up on amyloid beta immunotherapy for treating Alzheimer’s disease, it would be foolish to ignore the continued failures of antiamyloid approaches."

His commentary accompanies an article reporting disappointing results of the EXPEDITION3 trial of solanezumab, a humanized monoclonal antibody that has been designed to clear soluble Aβ from the brain.


 "There is a mountain of evidence supporting the concept that amyloid beta plays a pivotal role in Alzheimer's disease, but proposed treatments that target amyloid have thus far missed the mark. The field is clearly in need of innovative ideas."

"This shouldn't yet be the end of the road for antiamyloid therapy, which might still be effective as a preventative measure."

"The EXPEDITION3 trial raises the possibility that we need to focus on drugs that clear amyloid already deposited in the brain instead of trying to prevent its production." 

Murphy has worked as a researcher in the areas of aging and neurodegenerative disease for more than 20 years. His lab studies the production of the amyloid-β peptide (Aβ), the regulation of these processes, and how the peptide ultimately forms pathologic structures in the brain. Murphy has been involved in the development of several mouse models that are widely used for Alzheimer's research.

The Sanders-Brown Center on Aging is one of just 30 NIH-funded Alzheimer's Disease Centers and one of just nine continuously funded since the designation's inception in the mid-1980s.  Sanders-Brown is a world leader for research into Alzheimer's and other age-related dementias, credited with demonstrating that AD produces disease changes in the brain decades before symptoms occur and with the identification and naming of several diseases – called tauopathies --that are responsible for cognitive decline.

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