David G. Cook
Dept.: Research Associate Professor, Department of Medicine (Division of Gerontology and Geriatric Medicine)
Adjunct Research Associate Professor, Department of Pharmacology; Department of Psychiatry & Behavioral Science
Neuroscience Focus Groups: Cell and Molecular Neuroscience, Disorders of the Nervous System, Behavioral Neuroscience
Research: The Cook laboratory has two interrelated research programs
1. Mild traumatic brain injury (mTBI): Rapidly accumulating evidence indicates that repetitive exposure to the shock waves generated by high explosives initiate injury processes that cumulatively increase risk for neurodegenerative disorders similar to Alzheimer’s disease (AD), Parkinson’s disease (PD), and chronic traumatic encephalopathy (CTE). Our goal is to better understand the mechanisms of blast-induced brain injury by using a translationally relevant in vivo model systems approach to discover the mechanisms of repetitive mTBI. This work is closely integrated with ongoing clinical studies in individuals with blast-related mTBI. By this means we are working to integrate findings in model systems and humans using multi-modal neuroimaging, neuropathology, behavioral analyses, and molecular biology.
2. Alzheimer’s disease: AD is one of the most common disorders of aging and is a disease for which there very few therapeutic options—and those treatments currently available are of limited efficacy. The search for improved treatment options depends on attaining a better understanding of the mechanisms underlying AD pathogenesis. In this regard the Cook laboratory is focused on exploring the role astrocytes play in AD. Astrocytes are an abundant cell type in the brain that play critical roles in protecting neurons from injury, regulating cell-to-cell communication, and an array of key metabolic functions. In spite of their importance, their role in AD pathogenesis is not well understood. In recent years the Cook laboratory has uncovered new evidence of astrocyte dysfunction in AD centered on the failing ability of astrocytes to remove glutamate from the brain. The goal of this work is to understand how inefficient glutamate clearance occurs in AD so that we can devise new strategies to treat or prevent cognitive decline in AD.