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.