David L. Brody, M.D., Ph.D.

Dr. Brody is an MD, PhD trained, board certified neurologist with both a research specialization in neurodegenerative diseases and traumatic brain injury. Dr. Brody spends approximately 80% of his time performing research and 20% involved in clinical, teaching and administrative roles. Areas of active research include investigations of amyloid-beta and tau pathology in the setting of traumatic brain injury and Alzheimer’s disease, and advanced neuroimaging methods in traumatic brain injury. Dr. Brody maintains a well-funded, active laboratory in which a large volume of biochemical investigations, neuroimaging studies and experimental traumatic brain injury experiments are performed. There are currently 4 junior faculty members, 2 post-docs, 1 graduate student, 4 technicians, and 3 undergraduates in the lab.

Most relevant to the current application, Dr. Brody’s laboratory developed the first quantitative, high-throughput, specific assay for amyloid-beta oligomers; used this assay to differentiate brain tissue from demented patients with AD from non-demented patients with no overlap between groups, even when the non-demented patients had equal amounts of amyloid-beta plaque deposits (Esparza et al Annals of Neurology 2012); and performed the pioneering studies of the dynamics of amyloid-beta in the living human brain (Brody et al Science 2007). 

Funded Research

These projects were made possible from Cure Alzheimer's Fund support.

Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.

Wildburger, N. C., Esparza, T. J., LeDuc, R. D., Fellers, R. T., Thomas, P. M., Cairns, N. J., Kelleher, N. L., Bateman, R. J., & Brody, D. L. Diversity of amyloid-beta proteoforms in the Alzheimer’s disease brain, Scientific Reports, August 25, 2017, Read More

Esparza, T. J., Wildburger, N. C., Jiang, H., Gangolli, M., Cairns, N. J., Bateman, R. J., & Brody, D. L. Solble Amyloid-beta aggregates from human Alzheimr’s disease brains, Scientific Reports, December 5, 2016, Read More

Lebois, E. P., Schroeder, J. P., Esparza, T. J., Bridges, T. M., Lindsley, C. W., Conn, P. J., Brody, D. L., Daniels, J. S., & Levey, A. I. Disease-modifying effects of M-1 muscarinic acetylcholine receptor activation in an Alzheimer’s disease mouse model, ACS Chemical Neuroscience, June 21, 2017, Read More

Oberman, L. M., Exley, S., Philip, N. S., Siddiqi, S. H., Adamson, M. M., & Brody, D. L. Use of Repetitive Transcranial Magnetic Stimulation in the Treatment of Neuropsychiatric and Neurocognitive Symptoms Associated With Concussion in Military Populations, Journal of Head Trauma Rehabilitation, November 25, 2020, Read More

Tran, H. T., LaFerla, F. M., Holtzman, D. M., & Brody, D. L. Controlled cortical impact traumatic brain injury in 3xTg-AD mice causes acute intra-axonal amyloid beta accumulation and independently accelerates the development of tau abnormalities, Journal of Neuroscience, June 29, 2011, Read More

Schwetye, K. E., Cirrito, J. R., Esparza, T. J., Mac Donald, C. L., Holtzman, D. M., & Brody, D. L. Traumatic brain injury reduces solubl extracellular amyloid-beta in mice: a methodologically novel combined microdialysis-controlled cortical impact study, Neurobiology of Disease, December 1, 2010, Read More

Brody, D. L., Magnoni, S., Schwetye, K. E., Spinner, M. L., Esparza, T. J., Stocchetti, N., Zipfel, G. J., & Holtzman, D. M. Amyloid-beta dynamics correlate with neurological status in the injured human brain, Science, August 29, 2008, Read More

Brody, D. L., Jiang, H., Wildburger, N., & Esparza, T. J. Non-canonical soluble amyloid beta aggregates and plaque buffering: controversies and future direction for target discovery in Alzheier’s disease., Alzheimer's Research & Therapy, August 17, 2017, Read More

Esparza, T. J., Zhao, H., Cirrito, J. R., Cairns, N. J., Bateman, R. J., Holtzman, D. M., & Brody, D. L. Amyloid beta oligomerization in Alzheimer’s dementia versus high pathology controls, Annals of Neurology, January 1, 2013, Read More