Donald L. Price | Semantic Scholar

Publications
Influence

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ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions

Lucie I. Bruijn, Mark W. Becher, +8 authors Don W. Cleveland

Medicine, Biology

Neuron

1997 (First Publication: 1 February 1997)

High levels of familial Amyotrophic Lateral Sclerosis (ALS)-linked SOD1 mutants G93A and G37R were previously shown to mediate disease in mice through an acquired toxic property. We report here that… Expand

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 Drachman, Marshall F. Folstein, Robert Katzman., Donald L. Price, Emanuel M. Stadlan

Neurology

2011 (First Publication: 26 July 2011)

Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin.

Gabriele Schilling, Mark W. Becher, +11 authors David R Borchelt

Medicine, Biology

Human molecular genetics

1999 (First Publication: 1 March 1999)

Huntington's disease (HD) is an inherited, neurodegenerative disorder caused by the expansion of a glutamine repeat in the N-terminus of the huntingtin protein. To gain insight into the pathogenesis… Expand

An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria

Philip C. L. Wong, Carlos A Pardo, +6 authors Donald L. Price

Biology, Medicine

Neuron

1995 (First Publication: 1 June 1995)

Mutations in Cu/Zn superoxide dismutase (SOD1) cause a subset of cases of familial amyotrophic lateral sclerosis. Four lines of mice accumulating one of these mutant proteins (G37R) develop severe,… Expand

Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo

David R Borchelt, Gopal Thinakaran, +17 authors Sangram S Sisodia

Biology, Medicine

Neuron

1996 (First Publication: 1 November 1996)

Mutations in the presenilin 1 (PS1) and presenilin 2 genes cosegregate with the majority of early-onset familial Alzheimer's disease (FAD) pedigrees. We now document that the Abeta1-42(43)/Abeta1-40… Expand

Endoproteolysis of Presenilin 1 and Accumulation of Processed Derivatives In Vivo

Gopal Thinakaran, David R Borchelt, +14 authors Sangram S Sisodia

Biology, Medicine

Neuron

1996 (First Publication: 1 July 1996)

The majority of early-onset cases of familial Alzheimer's disease (FAD) are linked to mutations in two related genes, PS1 and PS2, located on chromosome 14 and 1, respectively. Using two highly… Expand

Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins

David R Borchelt, Tamara Ratovitski, +6 authors Sangram S Sisodia

Medicine, Biology

Neuron

1997 (First Publication: 1 October 1997)

Missense mutations in two related genes, termed presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees. In a variety of… Expand

Identification and localization of muscarinic acetylcholine receptor proteins in brain with subtype-specific antibodies

A. I. Levey, Cheryl A. Kitt, William F Simonds, Donald L. Price, Mark R. Brann

Biology, Medicine

1991 (First Publication: 1 October 1991)

mRNAs encoding five genetically distinct muscarinic ACh receptors are present in the CNS. Because of their pharmacological similarities, it has not been possible to detect the individual encoded… Expand

Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain.

Peter John Whitehouse, Donald L. Price, Robert G. Struble, Arthur W. Clark, Joseph T. Coyle, Marianne Delon

Medicine

Science

1982 (First Publication: 5 March 1982)

Recent evidence indicates that the nucleus basalis of Meynert, a distinct population of basal forebrain neurons, is a major source of cholinergic innervation of the cerebral cortex. Postmortem… Expand

BACE1, a Major Determinant of Selective Vulnerability of the Brain to Amyloid-β Amyloidogenesis, is Essential for Cognitive, Emotional, and Synaptic Functions

Fiona M. Laird, Huaibin Cai, +11 authors Philip C. L. Wong

Medicine, Biology

The Journal of Neuroscience

2005 (First Publication: 14 December 2005)

A transmembrane aspartyl protease termed β-site APP cleavage enzyme 1 (BACE1) that cleaves the amyloid-β precursor protein (APP), which is abundant in neurons, is required for the generation of… Expand