A Short Biography:
Bruce Teter received a B.S. in marine biology and a minor in chemistry from Cal. State U., Long Beach in 1982. Dr. Teter received a Ph.D. degree in molecular biology from the University of Southern California in 1991 studying DNA structure in control of protein binding and gene expression. He then completed a postdoctoral fellowship in neurogerontology focusing on epigenetic control of gene expression changes with aging, working with Dr. Caleb Finch at the Andrus Gerontology Center in the School of Gerontology at USC. In 1996 he joined the lab of Dr. Greg Cole at UCLA and is currently Adjunct Associate Professor in the Department of Neurology, and Chief of the ApoE Research Laboratory, and Research Associate at GRECC, Veterans Administration, GLAHS. Dr. Teter's research focuses on the neurobiology of apolipoprotein E (apoE),and how the apoE4 isotype is the major genetic risk factor for sporadic AD.
Dr. Teter's research focuses on the neurobiology of apolipoprotein E (apoE),and how the apoE4 isotype is the major genetic risk factor for sporadic AD. Dr. Teter has published seminal works showing how apoE4 inhibits neuroplasticity. His current research examines how apoE4 increases inflammation and modulates the innate immune system, both in the brain and in peripheral blood. These phenotypes are being examined for their role in pharmacogenetic effects of apoE4 on inhibiting the efficacy of therapeutic drugs, like the omega-3 fatty acid DHA found in fish oil, and the anti-inflammatory drug curcumin, a compound in curry spice. The goal is to find ways to overcome this apoE4 inhibition of drug efficacy, possibly through the addition of exercise.
A selected list of publications:
Life-span influences of apoE4 on CNS function. Invited Peer Commentary on: Schonheit, B., Glockner, F., and Ohm, T.G. (2006) Apolipoprotein E polymorphism and dendritic shape. ,
Neurobiology of Aging,
693-703; discussion 704-6..
Teter, B., Finch, C.E.
Caliban's Inheritance: Genetics of Neuronal Aging,
Trends in Neuroscience ,
Teter B, Xu P-T, Gilbert JR, Roses AD, Galasko D, Cole GM
Defective neuronal sprouting supported by human Apolipoprotein E4 represents a gain-of-deleterious function,
J. Neurosci. Res,
Teter B, Ashford JW
Neuroplasticity in Alzheimer's Disease,
Journal of Neuroscience Research,
2002; 70(Aging Brain and Alzheimer's Disease Special Issue):
Teter B, Raber J, Nathan B, Crutcher KA
The presence of apoE4, not the absence of apoE3, contributes to AD pathology,
J. Alzheimer's Disease,