Posts by Bradley T. Hyman, MD, PhD
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Tau Pathobiology Differs Among Individuals with Alzheimer's Disease
Researchers at Massachusetts General Hospital observed differences in the kinetics of tau aggregation across brain tissue samples from individuals with sporadic Alzheimer's disease, confirming and extending the concept of patient-specific characteristics of tau in this disease.
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Tau Seeding of Neurons Negatively Affects Neuronal Function
Marta Perez-Rando, PhD, and Bradley T. Hyman, MD, PhD, of the Alzheimer Research Unit, and colleagues demonstrated in an animal model that propagation of tau negatively affects neuronal synaptic and metabolic physiology in ways similar to changes previously observed in human Alzheimer's disease.
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Tau Seeding of Neurons Negatively Affects Neuronal Function
Marta Perez-Rando, PhD, and Bradley T. Hyman, MD, PhD, of the Alzheimer Research Unit, and colleagues demonstrated in an animal model that propagation of tau negatively affects neuronal synaptic and metabolic physiology in ways similar to changes previously observed in human Alzheimer's disease.
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Tau Molecular Diversity Contributes to Clinical Heterogeneity of Alzheimer's Disease
Tau bioactivity correlates with rate of progression of cognitive decline in Alzheimer's disease, supporting the prospect of tau suppression as a potential therapeutic appro
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New Tools Facilitate Analysis of Alzheimer's Disease Genetics and Genomics Data
Neuroscientists at Massachusetts General Hospital have developed advanced methods to analyze and visualize publicly available gene expression and genome-wide association data relevant to Alzheimer's disease—and are sharing them free online.
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Amyloid Beta and Tau Synergize to Impair Neural Circuits in Alzheimer's Disease
In living transgenic mice, the two major proteins involved in Alzheimer's disease, amyloid beta and tau, synergize to impair neural circuits—calling into question the pertinence of therapies that target one protein or the other.
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Tau Damages Neurons in Alzheimer's Disease by Disrupting Molecular Transport
Neurologists at Massachusetts General Hospital have determined that tau fibril formation, one of the pathological hallmarks of Alzheimer's disease, disrupts molecular transport in neurons—suggesting a potential new therapeutic strategy.
Biography
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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