NSAID inhibition of Alzheimer Pathogenesis: Role of DHA This study investigates impact of DHA depletion by diet and transgene in relation to post-synaptic deficits in relation to PI3-K and PAK signaling pathways.
Program-Project 1: Visualizing Brain A-Beta, Tau and Serotonin Receptor Densities.
This study investigates PET imaging probes for amyloid and tau and neurons using a 3x Tg rat and Tau transgenic mouse model.
Dr. Greg M. Cole is currently a Professor of Medicine and Neurology at UCLA where he is also the Associate Director of the UCLA Alzheimer's Center and Associate Director for Research at the Geriatric Research, Education and Clinical Center for the Greater Los Angeles Veterans Administration System. After receiving undergraduate degrees in Physics and Biochemistry from University of California at Berkeley and working in an immunology lab at Harvard Medical School, he returned to Berkeley for doctoral work on Alzheimer's and aging (under Professor emeritus Paola Timiras) and then moved to San Diego for postdoctoral work on Alzheimer's at UCSD. His work over the last two decades has been centered on the production and role of beta amyloid in Alzheimer's disease. Based in part on a series of screens in pre-clinical models, three compounds, R-flurbiprofen, curcumin and DHA are already in or under serious consideration for clinical trials. His recent papers investigate the potential for AD prevention with omega 3 fatty acid (DHA, docosahexaenoic acid from fish) and the curry spice extract, curcumin, to control inflammation and oxidative damage and act directly on insoluble amyloid fibrils in plaques and more soluble toxic species in vitro and in vivo. They also explore the role of omega 3 and other dietary fatty acids control the neuroprotective PI3-kinase>Akt pathway, synaptic protein loss, amyloid and cognitive deficits. Other recent contributions include the co-development of amyloid and tangle PET imaging probes with UCLA colleagues. Much of his work is based on an analysis of environmental risk factors, notably NSAIDs, fats and antioxidants and other anti-amyloid agents for efficacy in animal models for the disease. The primary goal of his lab is to develop safe and widely available methods for the prevention of Alzheimer's and possibly other degenerative diseases of aging.