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B. T. Hyman
Researcher at Harvard University
Publications - 61
Citations - 5047
B. T. Hyman is an academic researcher from Harvard University. The author has contributed to research in topics: Apolipoprotein E & Alzheimer's disease. The author has an hindex of 32, co-authored 60 publications receiving 4792 citations.
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Plaque-induced neurite abnormalities: implications for disruption of neural networks in Alzheimer's disease.
Roger B. Knowles,Claire Wyart,Sergey V. Buldyrev,Luis Cruz,Brigita Urbanc,Michael E. Hasselmo,H. E. Stanley,B. T. Hyman +7 more
TL;DR: It is proposed that this type of delay, played out among thousands of plaques throughout neocortical areas, disrupts the precise temporal firing patterns of action potentials, contributing directly to neural system failure and dementia.
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Adeno-associated virus vectors serotyped with AAV8 capsid are more efficient than AAV-1 or -2 serotypes for widespread gene delivery to the neonatal mouse brain.
TL;DR: AAV8 proved to be more efficient than AAV1 or AAV2 vectors for gene delivery to all of the structures analyzed, including the cerebral cortex, hippocampus, olfactory bulb, and cerebellum, indicating that AAV8 is the superior serotype for gene Delivery to the CNS.
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Reduced apolipoprotein ϵ4 allele frequency in the oldest old Alzheimer's patients and cognitively normal individuals
TL;DR: The data support two new conclusions: (1) the ApoE- ϵ4 associated risk for AD is age-dependent, probably due to censoring by the earlier development of AD in ApoN- ϴ4 individuals, and (2) despite the ApOE-π4 associatedrisk for AD, it is possible to reach extreme old age with normal cognition.
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Progression of cerebral amyloid angiopathy: accumulation of amyloid-beta40 in affected vessels.
TL;DR: Findings suggest that progression from asymptomatic to advanced CAA reflects progressive accumulation of amyloid in vessels previously seeded with amyloids, and that this process is selectively enhanced by apoliporprotein E ϵ4.
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Neuropathology and apolipoprotein E profile of aged chimpanzees: implications for Alzheimer disease
TL;DR: Findings militate against the hypothesis that the absence of APOE type 3 allele predisposes to neurofibrillary tangle formation and support the value of aged primates for exploring mechanisms of amyloid processing and the role of apoE.