T
Thomas N. Chase
Researcher at National Institutes of Health
Publications - 304
Citations - 20086
Thomas N. Chase is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Levodopa & Dopamine. The author has an hindex of 70, co-authored 304 publications receiving 19453 citations. Previous affiliations of Thomas N. Chase include St. Elizabeth Hospital & Bloomsburg University of Pennsylvania.
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The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS): Preliminary Clinical Validity
TL;DR: Data suggest that the RBANS is effective at both detecting and characterizing dementia of different etiologies, and is consistent with the neuropsychological profiles of these dementing disorders derived from lengthier standardized tests and experimental investigations.
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Alzheimer's disease: Focal cortical changes shown by positron emission tomography
Norman L. Foster,Thomas N. Chase,Paul Fedio,Nicholas J. Patronas,Rodney A. Brooks,Giovanni Di Chiro +5 more
TL;DR: In all subjects, verbal competency generally correlated with metabolic activity in the left frontal and temporal areas, while visuoconstructive test performance was linked to glucose utilization in the right parietal lobe.
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Limbic System Abnormalities Identified in Schizophrenia Using Positron Emission Tomography With Fluorodeoxyglucose and Neocortical Alterations With Deficit Syndrome
Carol A. Tamminga,Gunvant K. Thaker,Robert Buchanan,Brian Kirkpatrick,Larry Alphs,Thomas N. Chase,William T. Carpenter +6 more
TL;DR: The results suggest that the limbic system, especially the hippocampus, is functionally involved in schizophrenic psychosis and that different manifestations of schizophrenia may involve different neuronal circuits.
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D1 dopamine receptor activation required for postsynaptic expression of D2 agonist effects
TL;DR: The previously held view that D2 receptors alone are responsible for evoking the changes in behavior and basal ganglia output induced by nonselective dopamine agonists and endogenous dopamine is not supported by these results, which indicate that these phenomena require concurrent stimulation of both dopamine receptor subtypes.
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Degradation of α-Synuclein by Proteasome *
M. Catherine Bennett,John F. Bishop,Yan Leng,P. Boon Chock,Thomas N. Chase,M. Maral Mouradian +5 more
TL;DR: The degradation of both recombinant proteins and endogenous α-synuclein in these cells was blocked by the selective proteasome inhibitor β-lactone, indicating that both wild-type and A53T mutant α- synuclein are degraded by the ubiquitin-proteasome pathway.