Alzheimer's - Dementia, Author Interviews, Merck, NEJM / 10.04.2019

MedicalResearch.com Interview with: Michael F. Egan, MDVice President,  NeuroscienceGlobal Clinical DevelopmentMerck Research LaboratoriesNorth Wales, PAMichael F. Egan, MD Vice President,  Neuroscience Global Clinical Development Merck Research Laboratories North Wales, PA  MedicalResearch.com: What is the background for this study?   Response: Alzheimer’s disease (AD) appears to be due to the gradual accumulation of amyloid over many years (the “amyloid hypothesis”). At some point, it is thought that amyloid triggers abnormalities in tau, which then forms deposits within neurons and leads to progressive neurodegeneration. Amyloid is made up of  a small, sticky peptide, Abeta, which is produced when the enzyme BACE cleaves a large protein called APP.  In our trial, we tested whether a potent BACE inhibitor, verubecestat, could slow disease progression in subjects with early AD (or prodromal AD) by blocking formation of Abeta.  A previous trial in subjects with dementia due to AD failed to find evidence of efficacy. One possible reason for this failure is that subjects had too much amyloid in their brain already.