Diana R Kerwin
University of Texas Southwestern Medical Center, USA
Scientific Tracks Abstracts: J Neurol Neurosci
Drug development in Alzheimer′s disease has moved to development of disease-modifying therapies in early stage and pre-clinical disease. With the growing body of literature in the association of several mid-life risk factors that have been identified, several large scale, preventive studies are underway for the prevention of the memory and cognitive impairments due to Alzheimer′s disease neuropathology and neurodegeneration. In this presentation, several current and ongoing Phase 1,2 and 3 studies will be discussed, including safety and tolerability data of anti-amyloid and anti-tau monoclonal antibody therapies. There will also be a review of the current risk factors for development of AD and current state of understanding of the potential prevention of AD and related dementias.
Diana R Kerwin completed internal medicine residency and geriatric medicine fellowship training at Northwestern University Feinberg School of Medicine in Chicago, Ill, and specializes in cognitive disorders. Dr. Kerwin is the Director of the Texas Alzheimer’s and Memory Disorders program at Texas Health Presbyterian Hospital-Dallas and Assistant professor in the Department of Neurology and Neurotherapeutics at University of Texas Southwestern Medical Center in Dallas. Prior to founding the program in July 2013, she was Assistant Professor of Medicine-Geriatrics at Northwestern and faculty in the Northwestern University Cognitive Neurology and Alzheimer’s Disease Center (CNADC). Dr. Kerwin is the principal investigator on several Phase 1, 2 and 3 clinical trials for the development of therapeutics in Alzheimer’s and other dementias such as Progressive Supranuclear Palsy. She is the PI for several NIA funded studies on the prevention of Alzheimer’s disease, and collaborative studies for patients with frontotemporal lobe dementia syndromes. Dr. Kerwin’s areas of research and clinical interests include the prevention of cognitive decline and dementia.
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