D
Donald L. Price
Researcher at Johns Hopkins University
Publications - 471
Citations - 93184
Donald L. Price is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Cholinergic neuron & Senile plaques. The author has an hindex of 128, co-authored 471 publications receiving 90448 citations. Previous affiliations of Donald L. Price include Johns Hopkins University School of Medicine & Dartmouth–Hitchcock Medical Center.
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Journal ArticleDOI
Clinical diagnosis of Alzheimer's disease : report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease
Guy M. McKhann,David A. Drachman,Marshall F. Folstein,Robert Katzman,Donald L. Price,Emanuel M. Stadlan +5 more
TL;DR: The criteria proposed are intended to serve as a guide for the diagnosis of probable, possible, and definite Alzheimer's disease; these criteria will be revised as more definitive information becomes available.
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Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain.
Peter J. Whitehouse,Donald L. Price,Robert G. Struble,Arthur W. Clark,Joseph T. Coyle,Mahlon R. DeLong +5 more
TL;DR: Demonstration of selective degeneration of neurons of the nucleus basalis of Meynert represents the first documentation of a loss of a transmitter-specific neuronal population in a major disorder of higher cortical function and points to a critical subcortical lesion in Alzheimer's patients.
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Alzheimer's disease: a disorder of cortical cholinergic innervation
TL;DR: Advances in neurotransmitter systems involved in the symptomatic manifestations of neurological and psychiatric disorders reflect a close interaction between experimental and clinical neuroscientists in which information derived from basic neurobiology is rapidly utilized to analyze disorders of the human brain.
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Alzheimer disease: Evidence for selective loss of cholinergic neurons in the nucleus basalis
TL;DR: The nucleus basalis of Meynert provides diffuse cholinergic input to the neocortex and loss of this neuronal population may represent an anatomical correlate of the well‐documented cholinerential derangement in Alzheimer disease.
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Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo
David R. Borchelt,Gopal Thinakaran,Christopher B. Eckman,Christopher B. Eckman,Michael K. Lee,Frances Davenport,Tamara Ratovitsky,Cristian Mihail Prada,Grace Kim,Sophia Seekins,Debra Yager,Hilda H. Slunt,Rong Wang,Mary Seeger,Allan I. Levey,Sam Gandy,Neal G. Copeland,Nancy A. Jenkins,Donald L. Price,Steven G. Younkin,Steven G. Younkin,Sangram S. Sisodia +21 more
TL;DR: These studies provide compelling support for the view that one mechanism by which these mutant PS1 cause AD is by increasing the extracellular concentration of Abeta peptides terminating at 42(43), species that foster Abeta deposition.