Evidence map›Paper›PMID 29998118›Full record

ReviewMolecular neuropsychiatry2018

The Complex Interaction of Mitochondrial Genetics and Mitochondrial Pathways in Psychiatric Disease.

Ari B Cuperfain, Zhi Lun Zhang, James L Kennedy, Vanessa F Gonçalves

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular neuropsychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Female chronic social defeat stress (Frontiers in systems biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Integrating causal human genetics andFrontiers in molecular biosciences · 2025
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Research progress in mitochondrial quality control in schizophrenia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  19. Article
  20. The role of mitochondrial genome abundance in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    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

4 authors at 2 institutions in 1 country.

Ari B CuperfainDepartment of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
Zhi Lun ZhangDepartment of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
James L KennedyDepartment of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
Vanessa F GonçalvesDepartment of Psychiatry, University of Toronto, Toronto, Ontario, Canada.
University of Toronto · CACentre for Addiction and Mental Health · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While accounting for only 2% of the body's weight, the brain utilizes up to 20% of the body's total energy. Not surprisingly, metabolic dysfunction and energy supply-and-demand mismatch have been implicated in a variety of neurological and psychiatric disorders. Mitochondria are responsible for providing the brain with most of its energetic demands, and the brain uses glucose as its exclusive energy source. Exploring the role of mitochondrial dysfunction in the etiology of psychiatric disease is a promising avenue to investigate further. Genetic analysis of mitochondrial activity is a cornerstone in understanding disease pathogenesis related to metabolic dysfunction. In concert with neuroimaging and pathological study, genetics provides an important bridge between biochemical findings and clinical correlates in psychiatric disease. Mitochondrial genetics has several unique aspects to its analysis, and corresponding special considerations. Here, we review the components of mitochondrial genetic analysis - nuclear DNA, mitochon-drial DNA, mitochondrial pathways, pseudogenes, nuclear-mitochondrial mismatch, and microRNAs - that could contribute to an observable clinical phenotype. Throughout, we highlight psychiatric diseases that can arise due to dysfunction in these processes, with a focus on schizophrenia and bipolar disorder.

Indexed as

Bipolar disorderGene set analysisMitochondriaMitochondrial DNAMitochondrial dynamicsMitonuclear crosstalkOxidative phosphorylationSchizophrenia

Identifiers

PMID29998118
PMCPMC6032034
OpenAlexW2807237913

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.