12:00 – 1:00 pm
Sponsored by: The Mechanism of Aging and Dementia Training Program
Randy L. Buckner, Ph.D.
Professor of Psychology and of Neuroscience, Harvard University Director, Psychiatric Neuroimaging Research Program, Massachusetts General Hospital
Investigator, Howard Hughes Medical Institute
Randy L. Buckner is Professor of Psychology and of Neuroscience at Harvard University and affiliated with the Center for Brain Science. He is also the Director for Psychiatric Neuroimaging Research at the Massachusetts General Hospital. He received his B.A. degree in psychology and his M.A. and Ph.D. degrees in psychology and neuroscience from Washington University under the direction of Steven Petersen. He trained with Bruce Rosen as a postdoctoral fellow and then Instructor of Radiology at Harvard Medical School, where he pioneered new functional MRI methods to study human memory. Over the past decade his work has expanded to include studies of Alzheimer’s disease and neuropsychiatric illness. Professor Buckner has published over 100 scientific articles and chapters. He has received many awards including the Wiley Young Investigator Award from the Organization of Human Brain Mapping, the Young Investigator Award from the Cognitive Neuroscience Society, and the 2007 Troland Research Award from the National Academy of Sciences. Professor Buckner has been an investigator with the Howard Hughes Medical Institute since 2000.
Exploring Large-Scale Systems of the Human Brain and Their Importance for Understanding Aging and Alzheimer’s Disease
Information processing in the brain is accomplished by interactions among large-scale brain systems. Distinct areas possess specialized microarchitecture, anatomic connectivity, and functional response properties. At the broadest level, information processing in the cerebral cortex arises from this large array of specialized areas and how they interact to transform and propagate information. In this talk I will present a series of recent studies that have identified distinct large-scale brain systems in the human and dissociated their functional properties. One system, which involves the medial temporal lobe and a distributed set of association areas collectively known as the ‘default network’, is involved in remembering and is disrupted in Alzheimer’s disease. This network shows early atrophy in Alzheimer’s disease and metabolism reduction. A surprising observation has been that the default network is affected early by amyloid deposition in Alzheimer’s disease, including in preclinical cases, suggesting that properties of the network may facilitate the development of pathology.
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