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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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Human nerve growth factor prevents degeneration of basal forebrain cholinergic neurons in primates.

TL;DR: The rhNGF completely prevented alternation in the number and size of NGF receptor—and choline acetyltransferase—immunnoreactive neurons in the medical septal nucles and reversed atrophy in a subpopulation of large, basophilic medical which was previously used in the same primate lesion paradigm.
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Stable association of presenilin derivatives and absence of presenilin interactions with APP.

TL;DR: In situ chemical cross-linking and coimmunoprecipitation analyses are used to document that the N- and C-terminal derivatives of either PS1 or PS2 can be coisolated.
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Loss of pedunculopontine neurons in progressive supranuclear palsy.

TL;DR: The number of neurons within the lateral part of the pedunculopontine nucleus pars compacta (PPNc) was determined at six rostrocaudal levels in 3 subjects with progressive supranuclear palsy, in 9 subjects with Alzheimer's disease, and in 6 age‐matched control subjects.
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The Axonal Pathology in Chronic IDPN Intoxication

TL;DR: It is indicated that axonal atrophy occurs secondary to an impairment of slow axonal transport and suggested that a similar abnormality may underlie the pathological changes in certain other degenerative and toxic diseases of the nervous system.
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Motor Neuron Disease Occurring in a Mutant Dynactin Mouse Model Is Characterized by Defects in Vesicular Trafficking

TL;DR: Evidence is provided that autophagic cell death is implicated in the pathogenesis of mutant p150Glued mice and will be instrumental for not only clarifying disease mechanisms in ALS, but also for testing therapeutic strategies to ameliorate this devastating disease.