Bradley T. Hyman is the John B. Penney, Jr. Professor of Neurology at Harvard Medical School and Massachusetts General Hospital. He directs the Alzheimer's disease research unit at MassGeneral Institute for Neurodegenerative Diseases (MIND), with the goal of understanding the neuropathophysiologic and genetic factors that underlie dementia. Dr. Hyman's laboratory studies the anatomical and molecular basis of dementia in Alzheimer's disease and dementia with Lewy bodies. Dr. Hyman received his M.D. and Ph.D. from University of Iowa and he has received the Metropolitan Life Award, the Potamkin Prize, a National Institute on Aging Merit award, and an Alzheimer Association Pioneer Award. He is the current Director of the Massachusetts Alzheimer's Disease Research Center.
ResearchDr Hyman's research focuses on Alzheimer Disease and Lewy Body Dementias, spanning patient care, diagnostic and therapeutic issues, and neuropathology. He also directs a basic science program dedicated to understanding the underlying biology of dementias, how genetic risk factors impact the diease, and how to develop new therapies that may help patients.
(selected from >500 papers and chapters
1. de Calignon A, et al Casapse activation precedes and leads to tangles. Nature 2010 Apr 22;464(7292):1201-4
15. Serrano-Pozo A, et al Beneficial effect of human anti-amyloid-beta active immunization on neurite morphology and tau pathology. Brain. 2010 May;133(Pt 5):1312-27.
How jellyfish could potentially play a role in treatment
Neurofibrillary tangles - largely composed of tau protein- are one of the two pathological hallmarks of Alzheimer’s disease.
In this issue: spinal metastases & stereotactic radiosurgery; skull base tumors & endoscopic surgery; pediatric epilepsy dietary therapy; Alzheimer Disease: tau pathology; drug & gene discovery; early treatment; preclinical diagnostic tools.
A study led by MGH investigators shows that even low levels of the Alzheimer's-associated APOE4 protein can increase toxic amyloid beta brain plaques and the characteristic neuronal damage in mouse models of the disease. Introducing APOE2, a rare, potentially protective variant, reduced amyloid deposits and associated damage.
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