John B. Penney, Jr. Professor of Neurology, Massachusetts General Hospital
Neurology
Dr. Bradley T. Hyman, MD
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Bradley Hyman practices Neurology. He researched medicine at University of Iowa Carver College of Medicine. University of Iowa Carver College of Medicine is ranked 29/16 in Research/PrimaryCare. Bradley Hyman has written publications. He has 96 publications published with PubMed. The lastest publication is: 'The Feasibility of At-Home iPad Cognitive Testing For Use in Clinical Trials.' He is registered with Medicare.
Publications
- Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease.
- Multisite assessment of NIA-AA guidelines for the neuropathologic evaluation of Alzheimer's Disease.
- Exosome-associated AAV vector as a robust and convenient neuroscience tool.
- Alzheimer Disease: Alzheimer dementia with sparse amyloid-AD mimic or variant?
- Removing endogenous tau does not prevent tau propagation yet reduces its neurotoxicity.
- Tau PET imaging in aging and early Alzheimer's Disease.
- Alzheimer's Disease cerebrospinal fluid biomarker in cognitively normal subjects.
- Association between α-synuclein blood transcripts and early, neuroimaging-supported Parkinson's Disease.
- Genetic overlap between Alzheimer's Disease and Parkinson's Disease at the MAPT locus.
- Apolipoprotein E levels and Alzheimer risk.
- The Influence of Vascular Risk Factors and Stroke on Cognition in Late Life: Analysis of the NACC Cohort.
- APOEε2 is associated with milder clinical and pathological Alzheimer's Disease.
- FDA approved asthma therapeutic agent impacts amyloid β in the brain in a transgenic model of Alzheimer's Disease.
- Rarity of the Alzheimer Disease-Protective APP A673T Variant in the United States.
- Primary age-related tauopathy (PART): a common pathology associated with human aging.
- Carboxy Terminus Heat Shock Protein 70 Interacting Protein Reduces Tau-Associated Degenerative Changes.
- Effects of Multiple Genetic Loci on Age at Onset in Late-Onset Alzheimer Disease: A Genome-Wide Association Study.
- Genome-Wide Association Meta-analysis of Neuropathologic Features of Alzheimer's Disease and Related Dementias.
- At the interface of sensory and motor dysfunctions and Alzheimer's Disease.
- Failure analysis of clinical trials to test the amyloid hypothesis.
- Tau Propagation, Different Tau Phenotypes, and Prion-like Properties of Tau.
- The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer's Disease.
- Regulation of dynamin oligomerization in cells: the role of dynamin-actin interactions and its GTPase activity.
- Regional Cortical Thinning and Cerebrospinal Biomarkers Predict Worsening Daily Functioning Across the Alzheimer's Disease Spectrum.
- Methylene blue does not reverse existing neurofibrillary tangle pathology in the rTg4510 mouse model of tauopathy.
- Mild to moderate Alzheimer Dementia with insufficient neuropathological changes.
- Neurofibrillary tangle-bearing neurons are functionally integrated in cortical circuits in vivo.
- Examination of the clinicopathologic continuum of Alzheimer Disease in the autopsy cohort of the national Alzheimer coordinating center.
- The Role of Clusterin in Amyloid-β-Associated Neurodegeneration.
- APOE Genotype and Brain Development.
- Gene transfer of human apoe isoforms results in differential modulation of amyloid deposition and neurotoxicity in mouse brain.
- Soluble pathological tau in the entorhinal cortex leads to presynaptic deficits in an early Alzheimer's Disease model.
- The challenge of connecting the dots in the B.R.A.I.N.
- Propagation of tau pathology in Alzheimer's Disease: identification of novel therapeutic targets.
- Endogenous Tau Aggregates in Oligodendrocytes of rTg4510 Mice Induced by Human P301L Tau.
- Human LilrB2 is a β-amyloid receptor and its murine homolog PirB regulates synaptic plasticity in an Alzheimer's model.
- Reversal of Neurofibrillary Tangles and Tau-Associated Phenotype in the rTgTauEC Model of Early Alzheimer's Disease.
- Dissecting phenotypic traits linked to human resilience to Alzheimer's pathology.
- Mouse Gender Influences Brain Transduction by Intravascularly Administered AAV9.
- Tau - amyloid interactions in the rTgTauEC model of early Alzheimer's Disease suggest amyloid induced disruption of axonal projections and exacerbated axonal pathology.
- Studying synapses in human brain with array tomography and electron microscopy.
- Differential relationships of reactive astrocytes and microglia to fibrillar amyloid deposits in Alzheimer Disease.
- CSF biomarker variability in the Alzheimer's Association quality control program.
- Brain interstitial oligomeric amyloid β increases with age and is resistant to clearance from brain in a mouse model of Alzheimer's Disease.
- Microfluidic Chemotaxis Platform for Differentiating the Roles of Soluble and Bound Amyloid-β on Microglial Accumulation.
- Synaptic alterations in the rTg4510 mouse model of tauopathy.
- A Phenotypic Change But Not Proliferation Underlies Glial Responses in Alzheimer Disease.
- Improved Design of Prodromal Alzheimer's Disease Trials through Cohort Enrichment and Surrogate Endpoints.
- Alzheimer's Disease Risk Gene CD33 Inhibits Microglial Uptake of Amyloid Beta.
- EM Structure of the Ectodomain of Integrin CD11b/CD18 and Localization of Its Ligand-Binding Site Relative to the Plasma Membrane.
- Mechanisms of protein seeding in neurodegenerative Diseases.
- Calcineurin activation causes retinal ganglion cell degeneration.
- Neuronal activity and secreted amyloid ò lead to altered amyloid ò precursor protein and presenilin 1 interactions.
- Soluble forms of tau are toxic in Alzheimer's Disease.
- Orchestrated experience-driven Arc responses are disrupted in a mouse model of Alzheimer's Disease.
- The Synaptic Accumulation of Hyperphosphorylated Tau Oligomers in Alzheimer Disease Is Associated With Dysfunction of the Ubiquitin-Proteasome System.
- Stable Size Distribution of Amyloid Plaques Over the Course of Alzheimer Disease.
- Apolipoprotein E4 effects in Alzheimer's Disease are mediated by synaptotoxic oligomeric amyloid-β.
- Apoptotic and non-apoptotic roles of caspases in neuronal physiology and pathophysiology.
- Distinct dendritic spine and nuclear phases of calcineurin activation after exposure to amyloid-β revealed by a novel fluorescence resonance energy transfer assay.
- National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's Disease: a practical approach.
- Nanoparticles enhance brain delivery of blood-brain barrier-impermeable probes for in vivo optical and magnetic resonance imaging.
- Distinct Roles In Vivo for the Ubiquitin-Proteasome System and the Autophagy-Lysosomal Pathway in the Degradation of {alpha}-Synuclein.
- The SIST-M: Predictive Validity of a Brief Structured Clinical Dementia Rating Interview.
- Amyloid-β associated volume loss occurs only in the presence of phospho-tau.
- Neuropathological alterations in Alzheimer Disease.
- Association of SNCA with Parkinson: replication in the Harvard NeuroDiscovery Center Biomarker Study.
- Alzheimer's Disease: synapses gone cold.
- Tau Accumulation Causes Mitochondrial Distribution Deficits in Neurons in a Mouse Model of Tauopathy and in Human AD Brain.
- LRAD3, A Novel Low-Density Lipoprotein Receptor Family Member That Modulates Amyloid Precursor Protein Trafficking.
- Reactive Glia not only Associates with Plaques but also Parallels Tangles in Alzheimer's Disease.
- The Alzheimer's Association external quality control program for cerebrospinal fluid biomarkers.
- Amyloid-related imaging abnormalities in amyloid-modifying therapeutic trials: Recommendations from the Alzheimer's Association Research Roundtable Workgroup.
- Erratum to: Are Tangles as Toxic as They Look?
- Soluble tau Species, Not Neurofibrillary Aggregates, Disrupt Neural System Integration in a tau Transgenic Model.
- Characterization of oligomer formation of amyloid-{beta} peptide using a split-luciferase complementation assay.
- Are Tangles as Toxic as They Look?
- Plasma {beta}-Amyloid Linked to Cognitive Decline.
- The diagnosis of dementia due to Alzheimer's Disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines ...
- Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau trans...
- Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's Disease.
- Preoperative Cognitive Assessment of the Elderly Surgical Patient: A Call for Action.
- Amyloid-Dependent and Amyloid-Independent Stages of Alzheimer Disease.
- The Structured Interview & Scoring Tool-Massachusetts Alzheimer's Disease Research Center (SIST-M): development, reliability, and cross-sectional validation of a b...
- Calcineurin inhibition with FK506 ameliorates dendritic spine density deficits in plaque-bearing Alzheimer model mice.
- Monitoring protein aggregation and toxicity in Alzheimer's Disease mouse models using in vivo imaging.
- Studying protein degradation pathways in vivo using a cranial window-based approach.
- Ubiquitinylation of α-synuclein by carboxyl terminus Hsp70-interacting protein (CHIP) is regulated by Bcl-2-associated athanogene 5 (BAG5).
- Microscopic Imaging of Intracellular Calcium in Live Cells Using Lifetime-Based Ratiometric Measurements of Oregon Green BAPTA-1.
- Caspase activation without apoptosis: insight into Aβ initiation of neurodegeneration.
- Apolipoprotein E: isoform specific differences in tertiary structure and interaction with amyloid-β in human Alzheimer brain.
- Heat-shock protein 70 modulates toxic extracellular α-synuclein oligomers and rescues trans-synaptic toxicity.
- Antioxidants have a rapid and long-lasting effect on neuritic abnormalities in APP:PS1 mice.
- Novel Progranulin Mutation Detected in 2 Patients With FTLD.
- The Feasibility of At-Home iPad Cognitive Testing For Use in Clinical Trials.
Schools
Roy J Lucille a Carver College Of Medicine At University Of Iowa
University Iowa
Procedures Preformed
- EEG (Electroencephalogram)
Conditions Treated
- Alzheimer's Disease
- Convulsions
- Dementia
- Meningiomas
Doctors Specialties
- Neurology
Accepted Insurances
Education
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University of Iowa Hospitals and Clinics -
University of Iowa Carver College of Medicine
Hospital
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Massachusetts General Hospital
Drug Facts
| NPI NUMBER | 1659355238 | |
| NPPES Provider LastName | HYMAN | |
| NPPES Provider FirstName | BRADLEY | |
| NPPES Provider ZIPCode | 021143117 | |
| NPPES Provider State | MA | |
| Specialty Description | Neurology | |
| Total Claim Count | 150.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1659355238 |
| Last Name Of The Provider | HYMAN |
| First Name Of The Provider | BRADLEY |
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