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

Associate Professor,

Department of Neurology

Washington University School of Medicine

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

Project Description Researchers Funding
The Root of Alzheimer’s Disease: Purification and Characterization of Amyloid-beta Oligomers from the Human Brain

Large, poorly soluble aggregates of the amyloid-beta peptide form the senile plaques that are a pathological hallmark of Alzheimer’s disease, but the extent of plaque deposition correlates only moderately with dementia; for example many middle aged and elderly people have extensive plaque deposition without any signs of dementia. Instead, several types of smaller water soluble amyloid-beta oligomers have been found to be more toxic than either plaques or amyloid-beta peptide monomers.


Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.
Norelle C. Wildburger, Thomas J. Esparza, Richard D. LeDuc, Ryan T. Fellers, Paul M. Thomas, Nigel J. Cairns, Neil L. Kelleher, Randall J. Bateman, David L. Brody, Diversity of Amyloid-beta Proteoforms in the Alzheimer's Disease Brain, Scientific Reports, 7, 25 Aug 2017
David L. Brody, Hao Jiang, Norelle Wildburger, Thomas J. Esparza, Non-canonical soluble amyloid-beta aggregates and plaque buffering: controversies and future directions for target discovery in Alzheimer's disease, Alzheimers Research & Therapy, 9(1), 17 Aug 2017, 62
Evan P. Lebois, Jason P. Schroeder, Thomas J. Esparza, Thomas M. Bridges, Craig W. Lindsley, P. Jeffrey Conn, David L. Brody, J. Scott Daniels, Allan I. Levey, Disease-Modifying Effects of M-1 Muscarinic Acetylcholine Receptor Activation in an Alzheimer's Disease Mouse Model, Acs Chemical Neuroscience, 8(6), Jun 2017, 1177-1187
Octavian Adam, M.D., Christine L. Mac Donald, Ph.D., Dennis Rivet, M.D., John Ritter, M.D., Todd May, D.O., Maria Barefield, O.T.D., Josh Duckworth, M.D., Donald LaBarge, M.D., Dean Asher, M.D., Benjamin Drinkwine, M.D., Yvette Woods, Ph.D., Michael Connor, Psy.D. and David L. Brody, M.D., Ph.D., Clinical and imaging assessment of acute combat mild traumatic brain injury in Afghanistan, Neurology, 85(3), 21 July 2015, 219-227