Bruce T. Lamb

1985-1991 Molecular Biology University of Pennsylvania, Philadelphia, PA, United States 
 1991-1994 Cellular/Molecular Biology Johns Hopkins University, Baltimore, MD 
 1996-2005 Genetics Case Western Reserve University, Cleveland Heights, OH, United States 
 2005-2016 Neurosciences The Cleveland Clinic, Cleveland, OH, United States 
 2016- Stark Neurosciences Research Institute Indiana University School of Medicine, Indianapolis, IN, United States 
Alzheimer's disease, traumatic brain injury, neurodegeneration, animal models, drug discovery
"Bruce Lamb"

Dr. Lamb received his bachelor’s degree from Swarthmore College and his PhD from the University of Pennsylvania prior to a post-doctoral fellowship at Johns Hopkins University. In 1996, Dr. Lamb was recruited to Case Western Reserve University, where he rose from Assistant to Associate Professor. He joined the Cleveland Clinic in 2005 and rose to full Professor in 2011. In 2016, Dr. Lamb joined the Indiana University School of Medicine as Director of the Stark Neurosciences Research Institute. Dr. Lamb’s laboratory works on the basic and translational science of Alzheimer’s disease, with a focus on; animal models of Alzheimer’s disease (including Director of the IU/Jax/Pitt NIH-Funded Model Organism Development and Evaluation for Late-onset Alzheimer’s Disease program, MODEL-AD), discovery of new therapeutic targets (including Co-Director of the NIH-Funded IUSM/Purdue Alzheimer's Disease Drug Discovery Center), the role immune pathways in the development and progression of Alzheimer's disease and the the role of traumatic brain injury as an environmental modifier for the development of Alzheimer’s pathologies. In addition, Dr. Lamb is actively involved in advocacy for increased research funding for the disease. Dr. Lamb has received multiple honors including the National Civic Award and the Zaven Khachaturian Lifetime Achievement Award from the Alzheimer’s Association and was elected as a Fellow of the American Association for the Advancement of Science.
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Gunner G, Cheadle L, Johnson KM, et al. (2019) Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling. Nature Neuroscience
Bemiller SM, Maphis NM, Formica SV, et al. (2018) Genetically enhancing the expression of chemokine domain of CXCL1 fails to prevent tau pathology in mouse models of tauopathy. Journal of Neuroinflammation. 15: 278
Cheng-Hathaway PJ, Reed-Geaghan EG, Jay TR, et al. (2018) The Trem2 R47H variant confers loss-of-function-like phenotypes in Alzheimer's disease. Molecular Neurodegeneration. 13: 29
Katsumoto A, Miranda AS, Butovsky O, et al. (2018) Laquinimod attenuates inflammation by modulating macrophage functions in traumatic brain injury mouse model. Journal of Neuroinflammation. 15: 26
Tagge CA, Fisher AM, Minaeva OV, et al. (2018) Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model. Brain : a Journal of Neurology
Bemiller SM, McCray TJ, Allan K, et al. (2017) TREM2 deficiency exacerbates tau pathology through dysregulated kinase signaling in a mouse model of tauopathy. Molecular Neurodegeneration. 12: 74
Kokiko-Cochran ON, Saber M, Puntambekar S, et al. (2017) Traumatic brain injury in hTau model mice: Enhanced acute macrophage response and altered long-term recovery. Journal of Neurotrauma
Jay TR, Hirsch AM, Broihier ML, et al. (2017) Disease Progression-Dependent Effects of TREM2 Deficiency in a Mouse Model of Alzheimer's Disease. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience. 37: 637-647
Maphis N, Jiang S, Xu G, et al. (2016) Selective suppression of the α isoform of p38 MAPK rescues late-stage tau pathology. Alzheimer's Research & Therapy. 8: 54
Jay TR, Hirsch AM, Broihier ML, et al. (2016) Disease progression-dependent effects of TREM2 deficiency in a mouse model of Alzheimer's disease. The Journal of Neuroscience : the Official Journal of the Society For Neuroscience
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