- Clinical Interests
- Behavioral neurology
- Memory disorders
- Alzheimer's disease
- Medical Education
- PhD, University of Iowa Carver College of Medicine
- MD, University of Iowa College of Medicine
- Residency, University of Iowa Hospital & Clinics
- Board Certifications
- Boston: Massachusetts General Hospital
- Patient Gateway
- Yes, learn more
- Insurances Accepted
- Aetna Health Inc.
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- Blue Cross Blue Shield - Blue Care 65
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- Harvard Pilgrim Health Plan - ACD
- Harvard Pilgrim Health Plan - PBO
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- Humana/Choice Care PPO
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- OSW - Connecticut
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- United Healthcare (non-HMO) - ACD
- United Healthcare (non-HMO) - PBO
Note: This provider may accept more insurance plans than shown; please call the practice to find out if your plan is accepted.
- Patient Age Group
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.
- Research Summary
- Dr 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.
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
quotes MGH investigators Brad Hyman, Steven Arnold, Teresa Gomez-Isla and Rudy Tanzi
Neurology Bicentennial Celebration, 2011 Part II
Neurology Bicentennial Celebration, October 13, 2011. Clinical and research presentations on ALS, Stroke, Alzheimer’s Disease, and Parkinson’s Disease
15 Parkman Street
Boston, MA 02114-3117