Evidence map›Paper›PMID 24252612›Full record

ReviewBiochimica et biophysica acta2014

Mitochondrial genome changes and neurodegenerative diseases.

Milena Pinto, Carlos T Moraes

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Mitochondrial Inherited Disorders and their Correlation with Neurodegenerative Diseases.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
  6. Challenges and opportunities to bridge translational to clinical research for personalized mitochondrial medicine.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Unraveling heteroplasmy patterns with NOVOPlasty.NAR genomics and bioinformatics · 2020
    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

2 authors at 1 institution in 1 country.

Milena PintoDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, USA; Department of Cell Biology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Carlos T MoraesDepartment of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, USA; Neuroscience Graduate Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA; Department of Cell Biology, University of Miami Miller School of Medicine, Miami, FL 33136, USA. Electronic address: cmoraes@med.miami.edu.
University of Miami · US

Funding

SETTING THE STAGE FOR REPLACEMENT OF MITOCHONDRIAL GENESR01EY010804 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 1995 to 2025
$9.4M
Cellular and Molecular Consequences of Respiratory Chain Defects in NeuronsR01NS079965 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2012 to 2023
$3.9M
Mitochondrial Dysfunction in Neurodegeneration and Compensatory ApproachesR01AG036871 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MORAES, CARLOS TORRES · 2010 to 2020
$3.3M
NEI NIH HHS R01 EY010804NIA NIH HHS R01 AG036871NINDS NIH HHS R01 NS079965
6 · The paper itself

Abstract

Mitochondria are essential organelles within the cell where most of the energy production occurs by the oxidative phosphorylation system (OXPHOS). Critical components of the OXPHOS are encoded by the mitochondrial DNA (mtDNA) and therefore, mutations involving this genome can be deleterious to the cell. Post-mitotic tissues, such as muscle and brain, are most sensitive to mtDNA changes, due to their high energy requirements and non-proliferative status. It has been proposed that mtDNA biological features and location make it vulnerable to mutations, which accumulate over time. However, although the role of mtDNA damage has been conclusively connected to neuronal impairment in mitochondrial diseases, its role in age-related neurodegenerative diseases remains speculative. Here we review the pathophysiology of mtDNA mutations leading to neurodegeneration and discuss the insights obtained by studying mouse models of mtDNA dysfunction.

Indexed as

AnimalsDisease Models, AnimalDNA, MitochondrialGenome, MitochondrialHumansMitochondrial DiseasesNeurodegenerative DiseasesNeuronsDNA, MitochondrialEncephalopathyMitochondrionmtDNA

Identifiers

PMID24252612
PMCPMC4283582
OpenAlexW2000775246

What OpenQuestion holds

Textmetadata
LicenceTDM
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.