Bruce Teter, PhD


Research Lab

Associate Professor

UCLA Dept Medicine

Apolipoproteins, Estrogens, Aging

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. Future studies include evaluation of such drug effects on apoE expression, using anti-inflammatories and anti-oxidants.

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 1992, Dr. Teter was appointed Research Associate at the Andrus Gerontology Center. In 1996 he joined the lab of Dr. Greg Cole 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.


Dr. Teter has a strong background in aging, having studied under the esteemed professor & renowned biology of aging expert Professor Caleb Finch He joined UCLA under the direction of Dr. Greg Cole, and then acquired independent funding through the VA, Alzheimer Association, Dept Health and a KO1 training grant from NIH. He has been invited to several prestigious international and national conferences to speak on his original and cutting edge work on ApoE, and has been elected as Associate Editor on Neurobiology of Lipids and ad hoc reviewer for many prestigious journals. In the past six years, Dr. Teter’s has made intellectual contributions to UCLA by co-organizing two conferences (on neurodegenerative disorders and transgenic mice). He has expanded beyond the UCLA academic community and clearly established himself as a promising leader not only in his speciality field of ApoE biology but also in gerontology through continued interactions with current leaders in the field such as Caleb Finch at USC. His recent publications reflect this independence, excellent collaborative projects, and stature.  He has made important contributions to collaborative efforts with Dr. Cole based on co-authorship on publications in high impact journals. He has also been involved in ad hoc study sections for NIH.  He is well respected by other leaders in the field, as shown by invitation to speak at prestigious specialty conferences such as the Gordon Conferences.

  • Selected peer-reviewed publications (in chronological order). Do not include publications submitted or in preparation.

1.   Prentki, P., Teter, B., Chandler, M., and Galas, D. (1986) Functional Promoters Created by the Insertion of the Transposable Element IS1.  J. Molecular Biology 191: 383-393.

2. Teter, B., Osterburg, H.H., Anderson, C.P., and Finch, C.E. (1994) Methylation of the Rat Glial Fibrillary Acidic Protein Gene Shows Tissue-specific Domains. J. Neurosci. Res. 39:680-693.

3. Teter, B., Finch, C.E., and Condorelli, D. F. (1994) DNA Methylation in the Glial Fibrillary Acidic Protein Gene: Map of CpG Methylation Sites and Summary of Analysis by Restriction Enzymes and by LMPCR. J. Neurosci. Res. 39:708-709.

4. Laping, N.L., Nichols, N.R., Rozovsky, I.R., Teter, B., and Finch, C.E. (1994) Glial Fibrillary Acidic Protein: Regulation by Hormones, Cytokines, and Growth Factors. in "Symposium on GFAP", M. Brenner (ed.). Brain Pathology 4:259-275.

5. Laping, N.J., Anderson, C.P., O'Callaghan, J.P., Johnson, S.A., Teter, B., and Finch C.E. (1994) Age-Related Increases in Glial Fibrillary Acidic Protein are Not Associated with Changes in Transcription Rates or DNA Methylation in the Cerebral Cortex and Hippocampus of Male Rats. J. Neurosci. Res. 39:710-717.

6. Rozovsky, I.R., Teter, B., Laping, N.J., Krohn, K., O'Callaghan, J.P., Finch, C.E. (1995) Transcriptional Regulation of Glial Fibrillary Acidic Protein by Corticosterone in Rat Astrocytes in vitro is Influenced by Duration in Culture and by Neuron-Astrocyte Interactions. Endocrinology 136:2066-2073.

7. Teter, B., Anderson, C.P., Osterburg, H.H., Finch, C.E. (1996) Methylation of the Glial Fibrillary Acidic Protein Gene Shows Novel Biphasic Changes During Development. Glia, 17:195-205.

8. Yang, F. Sun, X., Beech, W., Teter, B., Wu, S., Sigel, J., Frautschy, S.A., Cole, G.M. (1998) Antibody to Caspase-Cleaved Actin Detects Apoptosis in Differentiated Neuroblastoma and Neurons and Plaque-Associated Neurons and Microglia in Alzheimer’s Disease.  American J. Pathology. 152:379-389.

9. Krohn, K.K., Rozovsky I.R., Teter B., Wals, P., Anderson, C.P., Finch, C.E. (1999) Glial fibrillary acidic protein transcriptional responses to Transforming Growth Factor-ß1 and Interleukin-1ß are mediated by an Nuclear Factor-1-like site in the near-upstream promoter. J. Neurochem. 72, 1353-1361.

10. 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.

11. 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.

12. Teter, B., Goodman S., Galas, D.J. (2000) DNA Bending and Twisting Properties of Integration Host Factor Determined by DNA Cyclization. Plasmid 43(1):73-84.

13.  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.

14. Teter, B. (2000) Apolipoprotein E isotype-specific effects in neurodegeneration. Alzheimer’s Reports 3:199-212.

15.  Harris-White, M., Chu, T., Miller, S.A., Simmons, M., Nash, D., Teter, B., Cole, G.M., Frautschy, S.A. (2001) Estrogen (E2) and glucocorticoid (Gc) effects on microglia and Aß clearance in vitro and in vivo.  Neurochemistry International 39 (5-6):435-448.

16. 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.

17. 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.

18. 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.

19. Cole, G.M., Morihara,T., Lim, G.P., Calon, F., Teter, B., Yang, F., Frautschy, S.A. (2003) Methods of Regulating Alzheimer Pathogenesis: Diet, Oxidative Damage and Inflammation. In Takeda, M. (ed.): Molecular Neurobiology of Alzheimer’s Disease and Related Disorders. pp. 1-16. Basel, Karger.

20. 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. Neuroscience23(3):167-79.

21. Teter, B., Finch, C.E. (2004) Caliban’s Inheritance: Genetics of Neuronal Aging. Trends in Neuroscience (10):627-32.

22. 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. Neuron43(5):633-45.

23. Zhao, L. Teter, B., Morihara, T., Lim, G., Ambegaokar, S. S.,  Ubeda, O., Frautschy, S.A., Cole, G.M. (2004) Insulin-degrading enzyme as a downstream target of insulin receptor signaling cascade: implications for Alzheimer’s disease intervention. J. Neuroscience 24:11120-11126.

24. Morihara, T., Teter, B., Lim, G., Yang, F., Frautschy, S.A., Ubeda, O., Beech, W., Boudinot, S., Boudinot, D., and Cole, G.M. (2005) Ibuprofen suppresses interleukin-1b induction of pro-amyloidogenic a-antichymotrypsin to ameliorate beta-amyloid (Aß)  pathology in Alzheimer's models. Neuropsychopharmacology .2005 Jun;30(6):1111-20.

25. Lim, G., Calon, F., Morihara, T., Yang, F., Teter, B., Ubeda, O., Salem N.Jr., Ashe, K.H., Frautschy, S.A., and Cole, G.M. (2005) A diet enriched diet enriched with the omega-3 fatty acid docosahexaenoic acid  (DHA) reduces amyloid burden in an aged Alzheimer mouse model. J. Neuroscience 25(12):3032-40

26. Cole, G.M., Lim, G., Yang, F.,Teter, B., Begum, A N., Ma, Q-L., Harris-White, M. E., Frautschy, S.A. (2005)  Prevention of Alzheimer’s disease: Omega-3 fatty acid and phenolic antioxidant interventions. Neurobiol. Aging Special Issue “Obesity, Diabetes, Mood, and Cognition: a SPARKS Workshop”. (in press).

Extracurricular activities include a disc jockey playing Early music/Classical Fiasco for the radio show KXLU 88.9 Sundays 7-9. He plays various bagpipes (French, Irish), and the Irish Whistle, Baroque Recorders, Krumhorn, and does harmonic singing in various groups.





| Contact Us | | Home | Help Us | Site |