Cure Alzheimer's Fund's Sam Sisodia and Charles Glabe named AAAS Fellows

Posted: Jan. 8, 2009

Dr. Sisodia of the University of Chicago and Dr. Gabe of the University of California at Irvine have been awarded the prestigious distinction of fellow of the American Association for the Advancement of Science (AAAS). Founded in 1848, AAAS is the world’s largest general scientific society and publisher of the journal Science.

Dr. Sisodia, a member of the Cure Alzheimer's Fund Research Consortium, is being recognized “for extraordinary contributions to understanding the function and dysfunction of APP and Presenilin 1 in cellular and animal models of Abeta amyloidosis in Alzheimer’s disease.”

Read more in the University of Chicago Chronicle

Dr. Glabe is also a member of the Cure Alzheimer’ Fund Research Consortium and a Professor of Molecular Biology & Biochemistry School of Biological Sciences at UC Irvine. He was one of 20 UC Irvine science and engineering researchers named as AAAS fellows, the largest class in 2008 of any university or institution in the United States.

Dr. Glabe’s research program is focused on amyloid structure and aggregation, in particular Aß, that is implicated as a causative agent of Alzheimer’s disease.  Dr. Glabe has recently discovered that prefibrillar oligomers, that represent intermediates in the fibril formation pathway, have a common structure that is recognized by a conformation-specific antibody. This antibody recognizes the oligomeric conformation of all amyloids tested and not the native conformation, random coil monomer or mature fibrillar amyloids regardless of protein sequence.  This discovery indicates that amyloids share a common structure and implies that they also share a common primary mechanism of amyloid oligomer pathogenesis.  Current work is focused on characterizing this common mechanism.

Charlie published an explanation of the importance of investigating Amyloid Oligomers in Cure Alzheimer’s Fund 2007 4th Quarter Report titled “Targeting Amyloid Oligomers in Alzheimer’s Disease”.