Browse by Medical Category
Accepting New Patients
Go To Programs
Note: This provider may accept more insurance plans than shown; please call the practice to find out if your plan is accepted.
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.
View my most recent publications at PubMed
(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.
MGH investigators have discovered a mechanism behind the spread of neurofibrillary tangles – one of the two hallmarks of Alzheimer's disease – through the brains of affected individuals. The research team found how an extremely version of the tau protein is able to spread from one neuron to another in the brains of Alzheimer's patients.
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.
How jellyfish could potentially play a role in treatment
Neurology Bicentennial Celebration, October 13, 2011. Clinical and research presentations on ALS, Stroke, Alzheimer’s Disease, and Parkinson’s Disease
Back to Top