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Bruce Lamb, Ph.D.

Professor, Medical and Molecular Genetics
Roberts Family Chair in Alzheimer's Disease Research
Executive Director, Stark Neurosciences Research Institute

Education/Training:
Ph.D., Molecular Biology, University of Pennsylvania, Philadelphia, PA (1991)
Post-Doc, Cellular/Molecular Biology, Johns Hopkins University, Baltimore, MD (1994)

Background:
In 1996, Dr. Lamb was recruited to Case Western Reserve University, where he rose from Assistant to Associate Professor and finally moved to the Cleveland Clinic in 2005.  At the Cleveland Clinic, Dr. Lamb was promoted from Associate Professor to Full Professor in 2011, and later was recruited to become the Executive Director of the Stark Neurosciences Research Institute with the IU School of Medicine in January 2016.

Dr. Lamb has received numerous awards and honors including the Jennifer B. Langston Award from the Cleveland Chapter of the Alzheimer’s Association and the National Civic Award and Zaven Khachaturian Lifetime Achievement Award from the National Alzheimer’s Association, is a Fellow in the American Association for the Advancement of Science and a member of the Medical and Scientific Advisory Council of the National Alzheimer’s Association.

Research:
Dr. Lamb’s laboratory works on the basic science of Alzheimer’s disease, with a focus on: 1) genetic modifiers identified from both mouse and human studies, 2) microglia and neuronal-microglial communication in the development and progression of AD pathologies; and 3) traumatic brain injury as an environmental modifier for the development of AD pathologies.  In addition, Dr. Lamb is actively involved in advocacy for increased research funding for the disease.

Search for Dr. Lamb on PubMed

Selected Publications:

  • Lamb, B.T., Sisodia, S.S., Lawler, A.M., Slunt, H.H., Kitt, C.A., Kearns, W.G., Pearson, P.L., Price, D.L., and J.D. Gearhart. Introduction and expression of the 400 kilobase amyloid precursor protein gene in transgenic mice. Nature Genet., 5:22-30, 1993.
  • Lamb, B.T., Call, L.M., Slunt, H.H., Bardel, K.A., Lawler, A.M., Eckman, C.B., Younkin, S.G., Holtz, G., Wagner, S.L., Price, D.L., Sisodia, S.S., and J.D. Gearhart. Altered metabolism of familial Alzheimer’s disease-linked amyloid precursor protein variants in yeast artificial chromosome mice. Hum. Mol. Genet., 6:1535-1541, 1997.
  • Lamb, B.T., Bardel, K.A., Kulnane, L.S., Anderson, J.J., Holtz, G., Wagner, S.L., Sisodia, S.S. and E.J. Hoeger. Amyloid production and deposition in mutant amyloid precursor protein and presenilin-1 yeast artificial chromosome transgenic mice. Nature Neurosci. 2:695-697, 1999. 
  • Hock, B.J., Lattal, M., Kulnane, L.S., Abel, T. and B.T. Lamb. Pathology associated memory deficits in Swedish mutant genome-based amyloid precursor protein transgenic mice. Curr Aging Sci, 2:205-213, 2009.
  • Lehman, E.J.H., Kulnane, L.S., Gao, Y., Petriello, M.C., Pimpis, K.M., Younkin, L., Dolios, G., Wang, R., Younkin, S.G., and B.T. Lamb. Genetic background regulates b-amyloid precursor protein processing and b-amyloid deposition in the mouse. Hum. Mol. Genet.,12:2949-2956, 2003.
  • Lehman, E.J.H., Kulnane, L.S., and B.T. Lamb. Alterations in b-amyloid production and deposition in brains regions of two transgenic models. Neurobiol. Aging, 24:645-653, 2003.
  • Chiocco, M.J., Kulnane, L.S., Younkin, L., Younkin, S., Evin, G., and B.T. Lamb. Altered amyloid-b metabolism and deposition in genomic-based b-secretase transgenic mice. J. Biol. Chem., 279:52535-52542, 2004, PMCID: PMC2659546.
  • Mann, K.M., Thorngate, F.E., Katoh-Fukui, Y., Hamanaka, H., Williams, D.L., Fujita, S., and B.T. Lamb. Independent effects of APOE on cholesterol metabolism and brain Ab levels in an Alzheimer’s disease mouse model. Hum. Mol. Genet., 13:1959-1968, 2004. 
  • Ryman, D., Gao, Y. and B.T. Lamb. Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer’s disease., Neurobiol. Aging, 29:1190-1198, 2008.
  • Yang, Y. Varvel, N.H., Lamb, B.T., and K. Herrup. Ectopic cell cycle events link human Alzheimer’s disease and amyloid precursor protein transgenic mouse models. J. Neurosci., 26:775-784, 2006.
  • Varvel, N.H., Bhaskar, K., Patil, A., Pimplikar, S.W., Herrup, K., and B.T. Lamb. Aβ oligomers induce neuronal cell cycle re-entry in Alzheimer’s disease. J. Neurosci., 28:10786-10793, 2008, PMCID: PMC2680286.
  • Varvel, N.H., Bhaskar, K., Kounnas, M.Z., Wagner, S.L., Yang, Y., Lamb, B.T., and K. Herrup. NSAIDs prevent, but do not reverse, neuronal cell cycle re-entry in Alzheimer’s disease mouse models. 119:3692-3702, J. Clin. Invest., 2009, PMCID: PMC2786797.
  • Bhaskar, K., Maphis, N., Xu, G.,, Varvel, N.H., Kokiko-Cochran, O.N., Weick, J.P., Staugaitis, S.M., Cardona, A., Ransohoff, R.M., Herrup, K., and B.T. Lamb. Microglial derived tumor necrosis factor-α drive Alzheimer’s disease-related neuronal cell cycle events. Neurobiol. Dis., 62:273-285, 2014, PMCID: PMC3877710.
  • Bhaskar, K., Konerth, M.E., Kokiko-Cochran, O.N., Cardona, A.E., Ransohoff, R.M., and B.T. Lamb. Regulation of tau pathology by the microglial fractakine receptor. Neuron, 68:19-31, 2010, PMCID: PMC2950825.
  • Lee, S., Xu, G., Jay, T.R., Bhatta, S., Kim, K.W., Jung, S., Landreth, G.E., Ransohoff, R.M., and B.T. Lamb. Opposing effects of membrane-anchored CX3CL1 on amyloid and tau pathologies via the p38 MAPK pathway. J. Neurosci., 34:12538-12546, 2014, PMCID: PMC4160782.
  • Kokiko-Cochran, O.N., Ransohoff, L., Veenstra, M., Lee, S., Saber, M., Sikora, M., Teknipp, R., Xu, G., Bemiller, S., Wilson, G., Crish, S., Bhaskar, K., Lee, Y.S., Ransohoff, R.M., and B.T. Lamb. Altered neuroinflammation and behavior following traumatic brain injury in a mouse model of Alzheimer’s disease. J. Neurotrauma, In Press, 2015, PMID: 26414955.
  • Jay, T.J., Miller, C.M., Cheng, P.J., Graham, L.C., Bemiller, S., Broihier, M.L., Xu, G., Margevicius, D., Karlo, J.C., Sousa, G.L., Cotleur, A.C., Butovsky, O., Bekris, L., Staugaitis, S.M., Leverenz, J.B., Pimplikar, S.W., Landreth, G.E., Howell, G.R., Ransohoff, R.M., and B.T. Lamb. TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models. J. Exp. Med., 212:287-295, 2015, PMCID: PMC4354365.
  • Savage, J.C., Jay, T.J., Goduni, E., Quigley, C., Mariani, M., Malm, T., Ransohoff, R., Lamb, B.T., and G. Landreth. Nuclear receptors license phagocytosis by Trem2+ myeloid cells in mouse models of Alzheimer’s disease. J. Neurosci., 35:6532-6543, 2015, PMID: 25904803.

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