Evidence map›Paper›PMID 28276496›Full record

ArticleScientific reports2017

Loss of forebrain MTCH2 decreases mitochondria motility and calcium handling and impairs hippocampal-dependent cognitive functions.

Antonella Ruggiero, Etay Aloni, Eduard Korkotian, Yehudit Zaltsman, Efrat Oni-Biton, Yael Kuperman, Michael Tsoory, Liat Shachnai, Smadar Levin-Zaidman, Ori Brenner and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. MTCH2 Suppresses Thermogenesis by Regulating Autophagy in Adipose Tissue.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Store-operated CaPNAS nexus · 2023
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

12 authors.

Antonella RuggieroDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.
Etay AloniDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Eduard KorkotianDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Yehudit ZaltsmanDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.
Efrat Oni-BitonDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Yael KupermanDepartment of Veterinary Resources, Weizmann Institute of Science, Rehovot 7610001, Israel.
Michael TsooryDepartment of Veterinary Resources, Weizmann Institute of Science, Rehovot 7610001, Israel.
Liat ShachnaiDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.
Smadar Levin-ZaidmanDepartment of Chemical research Support, Weizmann Institute of Science, Rehovot 7610001, Israel.
Ori BrennerDepartment of Veterinary Resources, Weizmann Institute of Science, Rehovot 7610001, Israel.
Menahem SegalDepartment of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Atan GrossDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot 7610001, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial Carrier Homolog 2 (MTCH2) is a novel regulator of mitochondria metabolism, which was recently associated with Alzheimer's disease. Here we demonstrate that deletion of forebrain MTCH2 increases mitochondria and whole-body energy metabolism, increases locomotor activity, but impairs motor coordination and balance. Importantly, mice deficient in forebrain MTCH2 display a deficit in hippocampus-dependent cognitive functions, including spatial memory, long term potentiation (LTP) and rates of spontaneous excitatory synaptic currents. Moreover, MTCH2-deficient hippocampal neurons display a deficit in mitochondria motility and calcium handling. Thus, MTCH2 is a critical player in neuronal cell biology, controlling mitochondria metabolism, motility and calcium buffering to regulate hippocampal-dependent cognitive functions.

Indexed as

AnimalsCalciumCognitionEnergy MetabolismFemaleHippocampusLocomotionLong-Term PotentiationMaleMaze LearningMiceMice, KnockoutMitochondriaMitochondrial Membrane Transport ProteinsNeuronsPostural BalanceCalciumMitochondrial Membrane Transport ProteinsMtch2 protein, mouse

Identifiers

PMID28276496
PMCPMC5343590

What OpenQuestion holds

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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.