Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 444

The DOI matches its Crossref record; 140 of the 140 references it cites were found in a registry or an index.

Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease

Open access
Nissanka, Nadee, Moraes, Carlos T.·2018·FEBS Letters

Abstract

Mitochondria are essential organelles within the cell where most ATP is produced through oxidative phosphorylation (OXPHOS). A subset of the genes needed for this process are encoded by the mitochondrial DNA (mt DNA). One consequence of OXPHOS is the production of mitochondrial reactive oxygen species (ROS), whose role in mediating cellular damage, particularly in damaging mt DNA during ageing, has been controversial. There are subsets of neurons that appear to be more sensitive to ROS‐induced damage, and mitochondrial dysfunction has been associated with several neurodegenerative disorders. In this review, we will discuss the current knowledge in the field of mt DNA and neurodegeneration, the debate about ROS as a pathological or beneficial contributor to neuronal function, bona fide mt DNA diseases, and insights from mouse models of mt DNA defects affecting the central nervous system.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1002/1873-3468.12956

Cites

140 of 140 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 140 references

Cited by

See all 444

Metadata

Authors
Nissanka, N., & Moraes, C. T.
Venue
FEBS Letters
Publisher
Wiley
Published
2018-01-09
Volume
592
Issue
5
Pages
728-742
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W2776177791
Cited by
444
References
140
FWCI
9.03
Type
journal article
Language
en
Open access
bronze

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease. https://app.cochat.ai/papers/10.1002/1873-3468.12956
The paper
Nissanka, N., & Moraes, C. T. (2018). Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease. FEBS Letters. https://doi.org/10.1002/1873-3468.12956

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.