Evidence map›Paper›PMID 23555730›Full record

ArticlePloS one2013

Intracranial injection of AAV expressing NEP but not IDE reduces amyloid pathology in APP+PS1 transgenic mice.

Nikisha Carty, Kevin R Nash, Milene Brownlow, Dana Cruite, Donna Wilcock, Maj-Linda B Selenica, Daniel C Lee, Marcia N Gordon, Dave Morgan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
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  4. Improving Gene Therapy for Angelman Syndrome with Secreted Human UBE3A.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
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  14. Spermidine/spermine-NAlzheimer's research & therapy · 2019
    Article
  15. Article
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  18. Review
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Nikisha CartyUniversity of South Florida College of Medicine, Byrd Alzheimer's Institute, Department of Molecular Pharmacology and Physiology, Tampa, Florida, United States of America.
Kevin R Nash
Milene Brownlow
Dana Cruite
Donna Wilcock
Maj-Linda B Selenica
Daniel C Lee
Marcia N Gordon
Dave Morgan
Florida College · USUniversity of South Florida · USUSF Health Byrd Alzheimer's Institute · USUniversity of Kentucky · US

Funding

AAV Gene Therapy for Alzheimer's DiseaseR01AG025509 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI MORGAN, DAVID · 2005 to 2009
$2.0M
NIA NIH HHS R01 AG025509
6 · The paper itself

Abstract

The accumulation of β-amyloid peptides in the brain has been recognized as an essential factor in Alzheimer's disease pathology. Several proteases, including Neprilysin (NEP), endothelin converting enzyme (ECE), and insulin degrading enzyme (IDE), have been shown to cleave β-amyloid peptides (Aβ). We have previously reported reductions in amyloid in APP+PS1 mice with increased expression of ECE. In this study we compared the vector-induced increased expression of NEP and IDE. We used recombinant adeno-associated viral vectors expressing either native forms of NEP (NEP-n) or IDE (IDE-n), or engineered secreted forms of NEP (NEP-s) or IDE (IDE-s). In a six-week study, immunohistochemistry staining for total Aβ was significantly decreased in animals receiving the NEP-n and NEP-s but not for IDE-n or IDE-s in either the hippocampus or cortex. Congo red staining followed a similar trend revealing significant decreases in the hippocampus and the cortex for NEP-n and NEP-s treatment groups. Our results indicate that while rAAV-IDE does not have the same therapeutic potential as rAAV-NEP, rAAV-NEP-s and NEP-n are effective at reducing amyloid loads, and both of these vectors continue to have significant effects nine months post-injection. As such, they may be considered reasonable candidates for gene therapy trials in AD.

Indexed as

SkullAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDependovirusFrontal LobeGene ExpressionGenetic TherapyHippocampusHumansInjectionsInsulysinMiceMice, TransgenicNeprilysinPresenilin-1Amyloid beta-PeptidesAmyloid beta-Protein PrecursorInsulysinNeprilysinPresenilin-1

Identifiers

PMID23555730
PMCPMC3610740
OpenAlexW2087986459

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.