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Bryce L. Sopher

Researcher at University of Washington

Publications -  66
Citations -  6873

Bryce L. Sopher is an academic researcher from University of Washington. The author has contributed to research in topics: Neurodegeneration & Ataxin 7. The author has an hindex of 38, co-authored 66 publications receiving 6463 citations. Previous affiliations of Bryce L. Sopher include University of Washington Medical Center & Michigan State University.

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The Werner syndrome protein is a DNA helicase.

TL;DR: It is reported that the Werner syndrome protein does indeed catalyze DNA unwinding and is homologous to members of the RecQ family of DNA helicases.
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Alzheimer’s Presenilin Mutation Sensitizes Neural Cells to Apoptosis Induced by Trophic Factor Withdrawal and Amyloid β-Peptide: Involvement of Calcium and Oxyradicals

TL;DR: In this article, the authors showed that expression of the human presenilin-1 L286V mutation in PC12 cells increases their susceptibility to apoptosis induced by trophic factor withdrawal and Abeta.
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Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice.

TL;DR: A direct link between a genetic defect that causes AD and excitotoxic neuronal degeneration is established, and new avenues for therapeutic intervention in AD patients are indicated.
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Deficient neurogenesis in forebrain-specific presenilin-1 knockout mice is associated with reduced clearance of hippocampal memory traces.

TL;DR: It is postulated that adult dentate neurogenesis may play a role in the periodic clearance of outdated hippocampal memory traces after cortical memory consolidation, thereby ensuring that the hippocampus is continuously available to process new memories.
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Increased Activity‐Regulating and Neuroprotective Efficacy of α‐Secretase‐Derived Secreted Amyloid Precursor Protein Conferred by a C‐Terminal Heparin‐Binding Domain

TL;DR: Findings indicate that alternative processing of βAPP has profound effects on the bioactivity of the resultant sAPP products and suggest that reduced levels of sAPPα could contribute to neuronal degeneration in Alzhiemer's disease.