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Dimitrios KAPOGIANNIS

Dimitrios Kapogiannis
Title: Deputy Laboratory Chief
Office(s): Human Neuroscience Section
Phone Number: 410-350-3953
Email Address: kapogiannisd@mail.nih.gov

Biography

Dimitrios Kapogiannis is a Clinician-Scientist who specializes in Alzheimer’s disease. He acquired his Medical Degree from the Medical School of the National and Kapodistrian University of Athens, Greece. Next, he completed a Neurology residency training program at the Massachusetts General Hospital/Brigham and Women’s Hospital/Harvard Medical School, and a Clinical Fellowship in Behavioral Neurology at the National Institute of Neurological Disorders and Stroke. He became an Investigator at the National Institute on Aging in 2014 and a Senior Investigator and Chief of the Human Neuroscience Section in 2021. He also holds an adjunct appointment as Associate Professor at the Department of Neurology of Johns Hopkins Medicine. He has authored more than 120 peer-reviewed publications and he is an Associate Editor of the “Journal of Extracellular Vesicles”, and member of the Editorial Boards of "Ageing Research Reviews", "npj Aging and Mechanisms of Disease", “Cells” and “Biomedicines”. His research includes basic, translational and clinical studies with a primary focus on Alzheimer’s disease and other aging-associated neurodegenerative disorders. He is widely recognized as an expert in the field of Extracellular Vesicle biomarkers and has pioneered the use of neuronal- and astrocytic-enriched subpopulations of plasma Extracellular Vesicles for the clinical and preclinical diagnosis of Alzheimer’s disease and other neurological and psychiatric diseases. He has also pioneered the use of plasma Extracellular Vesicles to demonstrate target engagement and biomarker responses in clinical trial in neurological and psychiatric disorders. Finally, Dr. Kapogiannis is interested in a range of clinical interventions (such as antidiabetic drugs, 5-2 calorie restriction and an oral ketone ester) that aim to decrease brain insulin resistance and change brain metabolism to mitigate Alzheimer’s-related pathogenic processes.

 

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