Evidence map›Paper›PMID 23525105›Full record

ArticleThe Journal of biological chemistry2013

Transcriptional regulation of insulin-degrading enzyme modulates mitochondrial amyloid β (Aβ) peptide catabolism and functionality.

María C Leal, Natalia Magnani, Sergio Villordo, Cristina Marino Buslje, Pablo Evelson, Eduardo M Castaño, Laura Morelli

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Synaptosomal bioenergetic defects are associated with cognitive impairment in a transgenic rat model of early Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  17. I - insulin transfer to mitochondria.Journal of bioenergetics and biomembranes · 2014
    Article
  18. Review
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

7 authors at 3 institutions in 1 country.

María C LealFundación Instituto Leloir, Instituto de Investigaciones Bioquímicas de Buenos Aires (Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET)), Avenida Patricias Argentinas 435, Ciudad Autónoma de Buenos Aires C1405BWE, Argentina.
Natalia Magnani
Sergio Villordo
Cristina Marino Buslje
Pablo Evelson
Eduardo M Castaño
Laura Morelli
Consejo Nacional de Investigaciones Científicas y Técnicas · ARFundación Instituto Leloir · ARUniversity of Buenos Aires · AR

Funding

A Natonal Resource for Postmortem Brain ResearchR24MH068855 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI BENES, FRANCINE M. · 2003 to 2012
$14.8M
NIMH NIH HHS R24 MH068855NIMH NIH HHS R24-MH 068855
6 · The paper itself

Abstract

Studies of post-mortem brains from Alzheimer disease patients suggest that oxidative damage induced by mitochondrial amyloid β (mitAβ) accumulation is associated with mitochondrial dysfunction. However, the regulation of mitAβ metabolism is unknown. One of the proteases involved in mitAβ catabolism is the long insulin-degrading enzyme (IDE) isoform (IDE-Met(1)). However, the mechanisms of its expression are unknown, and its presence in brain is uncertain. We detected IDE-Met(1) in brain and showed that its expression is regulated by the mitochondrial biogenesis pathway (PGC-1α/NRF-1). A strong positive correlation between PGC-1α or NRF-1 and long IDE isoform transcripts was found in non-demented brains. This correlation was weaker in Alzheimer disease. In vitro inhibition of IDE increased mitAβ and impaired mitochondrial respiration. These changes were restored by inhibition of γ-secretase or promotion of mitochondrial biogenesis. Our results suggest that IDE-Met(1) links the mitochondrial biogenesis pathway with mitAβ levels and organelle functionality.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsBrainHeat-Shock ProteinsHEK293 CellsHeLa CellsHumansInsulysinMitochondriaMitochondrial ProteinsNerve Tissue ProteinsNuclear Respiratory Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesHeat-Shock ProteinsInsulysinMitochondrial ProteinsNerve Tissue ProteinsNRF1 protein, humanNuclear Respiratory Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanPpargc1a protein, ratRNA-Binding ProteinsTranscription FactorsAmyloidMitochondrial MetabolismNeurodegenerationProteaseTranscription Factors

Identifiers

PMID23525105
PMCPMC3642335
OpenAlexW2080709676

What OpenQuestion holds

Textmetadata
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.