Dr. Greg M. Cole is currently a Professor of Medicine and Neurology at UCLA where he is also the Associate Director of the Mary Easton Alzheimer's Center at UCLA and Associate Director for Preclinical 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 a doctoral program on Alzheimer's and aging with Dr Paola Timiras and moved to San Diego for postdoctoral work on Alzheimer's at UCSD with Dr. Tsunao Saitoh. He is a recipient of the Cherkin Award for Research on Brain Aging.

Dr Cole’s research over the last two decades has been centered on the production and role of beta amyloid in Alzheimer's disease. He worked with Dr. K. Hsiao to develop the first successful academic transgenic mouse model for AD (1). Based in part on a series of screens in pre-clinical models from his group, four compounds, ibuprofen (2) R-flurbiprofen (4), curcumin (3,6) and DHA(5, 7) have advanced to clinical trials for Alzheimer’s. His recent papers investigate the potential for AD prevention with omega 3 fatty acid (DHA, docosahexaenoic acid from fish) and its role in preventing amyloid formation and abeta toxicity, notably through induction of the Alzheimer protective gene, SorLA (9) and prevention of insulin/neurotrophic factor resistance. His lab is also exploring the efficacy of the curry spice extract, curcumin, to control inflammation and oxidative damage and to act directly on insoluble amyloid fibrils in plaques and more soluble toxic species in vitro and in vivo. Dr. Cole and his colleague Dr. Sally Frautschy, have developed a much more bioavailable formulation of curcumin that is in current and planned clinical trials for both Alzheimer’s and cancer (10). The lab is also examining the role of omega 3 and other dietary fatty acids to control of a neuroprotective “insulin” or trophic factor signaling pathway (IR>IRS-1>PI3-kinase>Akt > GSK3 that is deranged in AD- as well as synaptic protein loss and abeta oligomer induced cognitive deficits. His group has presented evidence implicating aberrant activation of a “mental retardation” pathway as the mechanism underlying synaptic deficits in AD (8,11). Dr. Cole also works with Dr. Bruce Teter in the lab on role of Apolipoprotein E as a risk factor for Alzheimer’s disease and defective recovery after injury using transgenic mouse models and with Dr. Karen Gylys on synaptic defects analyzed by flow cytometry. Other recent contributions include a role in the development of an amyloid and tangle PET imaging probe with UCLA colleagues Drs G. Small and J. Barrio. Much of the work of the Cole and Frautschy labs is based on an analysis of environmental risk factors, notably NSAIDs, fats and antioxidants as well as development of other anti-amyloid agents in animal models for the disease. They are currently evaluating agents from a variety of sources including the Easton Drug Discovery Program using multiple animal models for Alzheimer’s 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.

References:
1. Hsiao, K., P. Chapman, S. Nilsen, C. Eckman, S. Younkin and G.M. Cole. Correlative Memory Deficits, Aß elevation and amyloid plaques in transgenic mice. Science 274:99-102, 1996.