Evidence map›Paper›PMID 17286867›Full record

ArticleMolecular neurodegeneration2007

APP-BP1 inhibits Abeta42 levels by interacting with Presenilin-1.

Yuzhi Chen, Angela M Bodles, Donna L McPhie, Rachael L Neve, Robert E Mrak, W Sue T Griffin

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Cellular Proteostasis in Neurodegeneration.Molecular neurobiology · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Cycle on Wheels: Is APP Key to the AppBp1 Pathway?Austin Alzheimer's and Parkinson's disease · 2014
    Article
  10. Article
  11. Neddylation dysfunction in Alzheimer's disease.Journal of cellular and molecular medicine · 2012
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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

6 authors at 3 institutions in 1 country.

Yuzhi ChenDepartment of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. chenyuzhi@uams.edu
Angela M Bodles
Donna L McPhie
Rachael L Neve
Robert E Mrak
W Sue T Griffin
University of Arkansas for Medical Sciences · USHarvard University · USMcLean Hospital · US

Funding

THE APOE-APP AXIS IN ALZHEIMER PATHOGENESISP01AG012411 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI GRIFFIN, SUE TILTON · 1995 to 2020
$25.0M
PHYSIOLOGICAL DISTURBANCES ASSOCIATED WITH NEONATAL INTRAVENTRICULAR HEMORRHAGEP20RR020146 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI GARCIA-RILL, EDGAR E. · 2004 to 2011
$17.2M
UAMS Alzheimer's Disease Core CenterP30AG019606 · NIA · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI BECK, CORNELIA MARIE · 2001 to 2005
$5.0M
NCRR NIH HHS P20 RR020146NIA NIH HHS P01 AG012411NIA NIH HHS P30 AG019606
6 · The paper itself

Abstract

backgroundThe beta-amyloid precursor protein (APP) is sequentially cleaved by the beta- and then gamma-secretase to generate the amyloid beta-peptides Abeta40 and Abeta42. Increased Abeta42/Abeta40 ratios trigger amyloid plaque formations in Alzheimer's disease (AD). APP binds to APP-BP1, but the biological consequence is not well understood.

resultsWe report that when the endogenous APP-BP1 was suppressed by small interfering RNAs (siRNAs), cell-associated Abeta42 was dramatically increased in APP695 expressing primary neurons. The accumulation of Abeta42 was accompanied by significant increases in APP and APP-CTF in APP-BP1 siRNA expressing neurons. In contrast, APP-BP1 overexpression in primary neurons significantly decreased the levels of Abeta and endogenous APP but not APLPs. We also investigated the potential mechanism of APP-BP1-mediated APP processing. APP-BP1 co-precipitated with Presenilin-1 (PS1) in native rat brain extracts, co-migrated with the gamma-secretase components in brain membrane extracts in glycerol gradient centrifugation, and colocalized in primary neurons. Further, the endogenous PS1-CTF was significantly downregulated by APP-BP1 expression.

conclusionOur data suggest that APP-BP1 may inhibit Abeta42 production by interacting with PS1 under physiological conditions.

Identifiers

PMID17286867
PMCPMC1802080
OpenAlexW2131682627

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Registered trials

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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.