Evidence map›Paper›PMID 21179577›Full record

ArticlePloS one2010

Amyloid-β triggers the release of neuronal hexokinase 1 from mitochondria.

Leonardo M Saraiva, Gisele S Seixas da Silva, Antonio Galina, Wagner S da-Silva, William L Klein, Sérgio T Ferreira, Fernanda G De Felice

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

56 citing papers in PubMed, 93 citations in OpenAlex.

  1. Trial
  2. Anti-kelch-like 12 and anti-hexokinase 1: novel autoantibodies in primary biliary cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2015
    Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
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  11. Article
  12. Article
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  15. Article
  16. Article
  17. Article
  18. Effect of Increased IL-1β on Expression of HK in Alzheimer's Disease.International journal of molecular sciences · 2021
    Article
  19. Review
  20. 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

7 authors at 2 institutions in 2 countries.

Leonardo M SaraivaPrograma de Bioquímica e Biofísica Celular, Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Gisele S Seixas da Silva
Antonio Galina
Wagner S da-Silva
William L Klein
Sérgio T Ferreira
Fernanda G De Felice
Universidade Federal do Rio de Janeiro · BRNorthwestern University · US

Funding

Abeta oligomers (ADDLs)in Alzheimers Disease pathologyR01AG022547 · NIA · NORTHWESTERN UNIVERSITY · PI KLEIN, WILLIAM L · 2003 to 2010
$1.9M
NEUROLOGICAL DEFICITS DUE TO TOXIC A BETA OLIGOMERSR01AG018877 · NIA · NORTHWESTERN UNIVERSITY · PI KLEIN, WILLIAM L · 2001 to 2003
$890k
NIA NIH HHS R01 AG018877NIA NIH HHS R01 AG022547NIA NIH HHS R01-AG18877NIA NIH HHS R01-AG22547
6 · The paper itself

Abstract

Brain accumulation of the amyloid-β peptide (Aβ) and oxidative stress underlie neuronal dysfunction and memory loss in Alzheimer's disease (AD). Hexokinase (HK), a key glycolytic enzyme, plays important pro-survival roles, reducing mitochondrial reactive oxygen species (ROS) generation and preventing apoptosis in neurons and other cell types. Brain isozyme HKI is mainly associated with mitochondria and HK release from mitochondria causes a significant decrease in enzyme activity and triggers oxidative damage. We here investigated the relationship between Aβ-induced oxidative stress and HK activity. We found that Aβ triggered HKI detachment from mitochondria decreasing HKI activity in cortical neurons. Aβ oligomers further impair energy metabolism by decreasing neuronal ATP levels. Aβ-induced HKI cellular redistribution was accompanied by excessive ROS generation and neuronal death. 2-deoxyglucose blocked Aβ-induced oxidative stress and neuronal death. Results suggest that Aβ-induced cellular redistribution and inactivation of neuronal HKI play important roles in oxidative stress and neurodegeneration in AD.

Indexed as

Amyloid beta-PeptidesAnimalsCell SurvivalCytosolDeoxyglucoseHexokinaseHumansIsoenzymesMitochondriaNeuronsOxidative StressRatsReactive Oxygen SpeciesTetrazolium SaltsThiazolesAmyloid beta-PeptidesDeoxyglucoseHexokinaseHK1 protein, humanIsoenzymesReactive Oxygen SpeciesTetrazolium SaltsThiazolesthiazolyl blue

Identifiers

PMID21179577
PMCPMC3002973
OpenAlexW2065714966

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.