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Neprilysin Gene Transfer Reduces Human Amyloid Pathology in Transgenic Mice

2003· article· en· 387 citations· W2155133303 on OpenAlex· 10.1523/jneurosci.23-06-01992.2003

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Opus teacher head0.058
GPT teacher head0.327
Teacher spread
0.269 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

The degenerative process of Alzheimer's disease is linked to a shift in the balance between amyloid-beta (Abeta) production, clearance, and degradation. Neprilysin has recently been implicated as a major extracellular Abeta degrading enzyme in the brain. However, there has been no direct demonstration that neprilysin antagonizes the deposition of amyloid-beta in vivo. To address this issue, a lentiviral vector expressing human neprilysin (Lenti-Nep) was tested in transgenic mouse models of amyloidosis. We show that unilateral intracerebral injection of Lenti-Nep reduced amyloid-beta deposits by half relative to the untreated side. Furthermore, Lenti-Nep ameliorated neurodegenerative alterations in the frontal cortex and hippocampus of these transgenic mice. These data further support a role for neprilysin in regulating cerebral amyloid deposition and suggest that gene transfer approaches might have potential for the development of alternative therapies for Alzheimer's disease.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Journal of Neuroscience
Topic
Autism Spectrum Disorder Research
Field
Neuroscience
Canadian institutions
Funders
National Institute on AgingParkinsonfondenAlzheimer's AssociationWayne and Gladys Valley FoundationCanadian Institutes of Health ResearchNational Parkinson FoundationNational Institutes of Health
Keywords
NeprilysinGenetically modified mouseTransgeneAmyloid (mycology)HippocampusAmyloidosisAmyloid precursor proteinAmyloid betaAlzheimer's diseaseNeurosciencePathologyBiologyMedicineDiseaseGeneBiochemistryEnzyme
Has abstract in OpenAlex
yes