Research uncovers new insights on ALS and points to a potentially promising treatment strategy
Blocking tau, a hallmark of Alzheimer’s disease, may benefit ALS patients.
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.
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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 disease, and how to develop new therapies that may help patients.
(selected from >500 papers and chapters
1. de Calignon A, et al Caspase 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.
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Blocking tau, a hallmark of Alzheimer’s disease, may benefit ALS patients.
Results could improve ALS detection and treatment.
Los investigadores han utilizado una estrategia de ingeniería genética para reducir drásticamente los niveles de tau—una proteína clave que se acumula y se enreda en el cerebro durante el desarrollo de la enfermedad de Alzheimer—en un modelo animal de la enfermedad.
Researchers have used a genetic engineering strategy to dramatically reduce levels of tau—a key protein that accumulates and becomes tangled in the brain during the development of Alzheimer’s disease—in an animal model of the condition.
A new study reveals a possible biological reason that Alzheimer’s Disease progresses at different rates in different patients.
Neurofibrillary tangles - largely composed of tau protein- are one of the two pathological hallmarks of Alzheimer’s disease.