The BACE‐1 inhibitor CNP520 for prevention trials in Alzheimer's disease
Ulf Neumann; Mike Ufer; Laura H. Jacobson; Marie‐Laure Rouzade‐Dominguez; Gunilla Huledal; Carine Kolly; Rainer M. Lüönd; Rainer Machauer · 2018 · EMBO Molecular Medicine
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
The beta‐site amyloid precursor protein cleaving enzyme‐1 (BACE‐1) initiates the generation of amyloid‐β (Aβ), and the amyloid cascade leading to amyloid plaque deposition, neurodegeneration, and dementia in Alzheimer's disease (AD). Clinical failures of anti‐Aβ therapies in dementia stages suggest that treatment has to start in the early, asymptomatic disease states. The BACE‐1 inhibitor CNP520 has a selectivity, pharmacodynamics, and distribution profile suitable for AD prevention studies. CNP520 reduced brain and cerebrospinal fluid (CSF) Aβ in rats and dogs, and Aβ plaque deposition in APP
Abstract by Ulf Neumann; Mike Ufer; Laura H. Jacobson; Marie‐Laure Rouzade‐Dominguez; Gunilla Huledal; Carine Kolly; Rainer M. Lüönd; Rainer Machauer, EMBO Molecular Medicine (2018) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.15252/emmm.201809316
