Evidence map›Paper›PMID 28595361›Full record

ArticleHuman molecular genetics2017

Mitochondrial dysfunction underlies cognitive defects as a result of neural stem cell depletion and impaired neurogenesis.

Mireille Khacho, Alysen Clark, Devon S Svoboda, Jason G MacLaurin, Diane C Lagace, David S Park, Ruth S Slack

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 3 pooled it
4.4field-weighted citation impact, top 5% 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

108 citing papers in PubMed, 3 syntheses or guidelines pooled it, 185 citations in OpenAlex.

  1. Pooled it
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  11. Expanding the cognitive spectrum of mitochondrial diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  12. Charting Brain Structure in 22q11.2 Deletion Syndrome with Clinical Neuroimaging.medRxiv : the preprint server for health sciences · 2026
    Article
  13. Article
  14. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
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48 more citing papers are in PubMed but not listed here.

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 1 country.

Mireille KhachoDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
Alysen ClarkDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
Devon S SvobodaDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
Jason G MacLaurinDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
Diane C LagaceDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
David S ParkDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
Ruth S SlackDepartment of Cellular and Molecular Medicine, University of Ottawa Brain and Mind Research Institute, Ottawa, ON K1H 8M5, Canada.
University of Ottawa · CAuOttawa Brain and Mind Research Institute

Funding

CIHR
6 · The paper itself

Abstract

Mitochondrial dysfunction is a common feature of many genetic disorders that target the brain and cognition. However, the exact role these organelles play in the etiology of such disorders is not understood. Here, we show that mitochondrial dysfunction impairs brain development, depletes the adult neural stem cell (NSC) pool and impacts embryonic and adult neurogenesis. Using deletion of the mitochondrial oxidoreductase AIF as a genetic model of mitochondrial and neurodegenerative diseases revealed the importance of mitochondria in multiple steps of the neurogenic process. Developmentally, impaired mitochondrial function causes defects in NSC self-renewal, neural progenitor cell proliferation and cell cycle exit, as well as neuronal differentiation. Sustained mitochondrial dysfunction into adulthood leads to NSC depletion, loss of adult neurogenesis and manifests as a decline in brain function and cognitive impairment. These data demonstrate that mitochondrial dysfunction, as observed in genetic mitochondrial and neurodegenerative diseases, underlies the decline of brain function and cognition due to impaired stem cell maintenance and neurogenesis.

Indexed as

AnimalsApoptosis Inducing FactorBrainCell DifferentiationCell ProliferationCognitionCognitive DysfunctionHumansMiceMice, TransgenicMitochondriaNeural Stem CellsNeurodegenerative DiseasesNeurogenesisNeuronsSignal TransductionAIFM1 protein, humanApoptosis Inducing Factor

Identifiers

PMID28595361
PMCPMC5886206
OpenAlexW2624475221

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.