Bruce Teter, Ph.D.

Titles

Associate Professor, Geriatric Medicine

Member, Brain Research Institute

Adjunct Associate Professor, Neurology

Contact Information

Email
bteter@ucla.edu
Phone
Cell-phone Number: 3104131759
Fax Number: 3102684855
Work Phone Number: 3104783711x42543
Address

Mailing Address:

VA Greater Los Angeles Healthcare System, West Los Angeles
Research
11301 Wilshire Blvd
Los Angeles, CA 90073
UNITED STATES

Work Address:

Office
UCLA-VAMC
mc151
16111 Plummer St.
Sepulveda, CA 91343
UNITED STATES
Laboratory
SEPUL VAMC 7
Los Angeles, CA 90095
UNITED STATES

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, Los Angeles, in 1991. He then completed a postdoctoral fellowship in neurogerontology working with Dr. Caleb Finch at the Andrus Gerontology Center in the School of Gerontology at USC. In 1992, Dr. Teter was appointed Research Associate at the Andrus Gerontology Center. In 1996 he joined the lab of Dr. Greg Cole at UCLA and is currently Associate Professor in the Department of Medicine at UCLA, and Chief of the ApoE Research Laboratory, and Research Associate at GRECC, Veterans Administration, GLAHS.

Publications

Teter, B.   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, 2006; in press: .
Teter, B., Finch, C.E.   Caliban's Inheritance: Genetics of Neuronal Aging, Trends in Neuroscience , 2004; 10: 627-32.
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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, 2002; (687): 331-336.
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Teter B, Ashford JW   Neuroplasticity in Alzheimer's Disease, Journal of Neuroscience Research, 2002; 70(Aging Brain and Alzheimer's Disease Special Issue): 402-437.
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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, 2002; (4): 155-163.