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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Bruce
Last Name:Teter
Title:Associate Professor
Advanced Degrees:Ph.D.
Affiliation:UCLA, VAMC
Department:Medicine
Street Address 1:UCLA-VAMC, mc151
Street Address 2:16111 Plummer St.
City:Sepulveda
State/Province:CA
Zip/Postal Code:91343
Country/Territory:U.S.A.
Phone:8188917711x7481
Fax:8188955835
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 13 September 2010]
View all comments by Bruce Teter
Clinical Interests:
Alzheimer Disease, Parkinson Disease
Research Focus:
Molecular and Cell biology, Neurobiology, Clinical trials, Oxidative Stress, Bioinformatics/Statistics, Signal transduction, Genetics, DNA microarrays, Animal Models
Work Sector(s):
University
Web Sites:
Personal: http://faculty.bri.ucla.edu/institution/personnel?personnel%5fid=46155
Professional: http://neurobiologyoflipids.org/editors/bruceteter.html
Lab: http://alzheimer.neurology.ucla.edu/
Researcher Bio
Dr. Teter's research focuses on the neurobiology of apolipoprotein E (apoE), the mechanisms of regeneration in the brain, and the role this may play in neurodegeneration of Alzheimer's (AD) .

ApoE is the major genetic risk factor for sporadic AD. The apoE4 isotype may accelerate the age of onset of AD by inhibiting compensatory regenerative responses like neuronal sprouting, possibly as a consequence of its role in lipid metabolism or cellular signaling. Studies using organotypic hippocampal slice cultures from apoE transgenic mice have shown that apoE4 represents a gain-of-negative activity in supporting neuronal sprouting. This may have important implications for the pharmacogenetic efficacy of therapeutic drugs for AD that modulate the expression of the apoE gene. Current studies include evaluation of such drug effects on apoE expression, using anti-inflammatories and anti-oxidants, and studies on the cellular signaling properties of apoE.
Top Papers
Teter, B., Beech, W., Harris-White, M., Frautschy, S.A., Cole, G.M. (1999) Role of Apolipoprotein E and Estrogen in Mossy Fiber Sprouting in Hippocampal Slice Cultures. Neuroscience 91:1009-1016.
Teter, B., Xu, P-T, Gilbert, J. R., Roses, A. D., Galasko, D., Cole, G. M. (1999) Human Apolipoprotein E Isoform-Specific Differences in Neuronal Sprouting in Organotypic Hippocampal Slice Culture. J. Neurochem. 73: 2613-2616.
Lim, G.P., Yang, F., Chu, T., Chen, P., Beech, W., Teter, B., Tran, T., Ubeda, O., Hsiao-Ashe, K., Frautschy, S.A., Cole, G.M. (2000) Ibuprofen suppresses plaque pathology and inflammation in a mouse model of Alzheimer’s disease. J. Neuroscience 20:5709-5714.
Teter, B. (2000) Apolipoprotein E isotype-specific effects in neurodegeneration. Alzheimer’s Reports 3:199-212.
Teter, B., Xu, P-T., Gilbert, J. R., Roses, A. D., Galasko, D., Cole, G. M. (2002) Defective neuronal sprouting supported by human Apolipoprotein E4 represents a gain-of-deleterious function. J. Neurosci. Res. 687: 331-336.
Teter, B., Raber, J., Nathan, B., Crutcher, K.A. (2002) The presence of apoE4, not the absence of apoE3, contributes to AD pathology. J. Alzheimer’s Disease 4: 155-163.
Teter, B., Ashford, J.W. (2002) Neuroplasticity in Alzheimer’s Disease. In "Aging Brain and Alzheimer’s Disease," a Special Issue of Journal of Neuroscience Research. J. Neurosci. Res., 70: 402-437.
Teter, B. (2004) ApoE-dependent Plasticity in Alzheimer's Disease. Perspectives from the conference, Catalyst Conference on ApoE Therapeutics: Apolipoprotein E as a Target for Developing New Therapeutics for Alzheimer’s Disease. Institute for the Study of Aging (ISOA). New York Academy of Sciences, New York, NY. May 29-30, 2003. J. Mol. Neuroscience 23(3):167-79.
Teter, B., Finch, C.E. (2004) Caliban’s Inheritance: Genetics of Neuronal Aging. Trends in Neuroscience (10):627-32.
Calon, F., Lim, G., Yang, F., Morihara, T., Teter, B., Ubeda, O., Rostaing, P., Triller, A., Salem N.Jr., Ashe, K.H., Frautschy, S.A., and Cole, G.M. (2004) Docosahexaenoic acid protects from dendritic pathology in an Alzheimer’s disease mouse model. Neuron 43(5):633-45.

What is the greatest void to date in our knowledge of Alzheimer's Disease?
how does apoE isotype influence disease risk?
What is your leading hypothesis?
neuroplasticity failure causes the disease
(http://www.medafile.com; Teter, B., Ashford, J.W. (2002) Neuroplasticity in Alzheimer’s Disease. In "Aging Brain and Alzheimer’s Disease," a Special Issue of Journal of Neuroscience Research. J. Neurosci. Res., 70: 402-437.
What piece of missing evidence would help prove it?
apoE4 risk acts through failed neurplasticity
What is your fallback position?
mitochondrial defects

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