Evidence map›Paper›PMID 23216311›Full record

ReviewAntioxidants & redox signaling2013

Mitochondrial DNA oxidative damage and repair in aging and Alzheimer's disease.

Renato X Santos, Sónia C Correia, Xiongwei Zhu, Mark A Smith, Paula I Moreira, Rudy J Castellani, Akihiko Nunomura, George Perry

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing 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

96 citing papers in PubMed.

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  18. Efficacy of verbascoside, echinacoside, crenatoside on altitude-induced fatigue in rats and possible mechanism.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023
    Article
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  20. Review

36 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

8 authors.

Renato X SantosCenter for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Sónia C Correia
Xiongwei Zhu
Mark A Smith
Paula I Moreira
Rudy J Castellani
Akihiko Nunomura
George Perry

Funding

RCMI Center for Interdiscplinary Health Research CIHRG12MD007591 · NIMHD · UNIVERSITY OF TEXAS SAN ANTONIO · PI PERRY, GEORGE · 2012 to 2016
$10.4M
NIMHD NIH HHS G12 MD007591NIMHD NIH HHS G12MD007591
6 · The paper itself

Abstract

significanceMitochondria are fundamental to the life and proper functioning of cells. These organelles play a key role in energy production, in maintaining homeostatic levels of second messengers (e.g., reactive oxygen species and calcium), and in the coordination of apoptotic cell death. The role of mitochondria in aging and in pathophysiological processes is constantly being unraveled, and their involvement in neurodegenerative processes, such as Alzheimer's disease (AD), is very well known. RECENT ADVANCES: A considerable amount of evidence points to oxidative damage to mitochondrial DNA (mtDNA) as a determinant event that occurs during aging, which may cause or potentiate mitochondrial dysfunction favoring neurodegenerative events. Concomitantly to reactive oxygen species production, an inefficient mitochondrial base excision repair (BER) machinery has also been pointed to favor the accumulation of oxidized bases in mtDNA during aging and AD progression. CRITICAL ISSUES: The accumulation of oxidized mtDNA bases during aging increases the risk of sporadic AD, an event that is much less relevant in the familial forms of the disease. This aspect is critical for the interpretation of data arising from tissue of AD patients and animal models of AD, as the major part of animal models rely on mutations in genes associated with familial forms of the disease. FUTURE DIRECTIONS: Further investigation is important to unveil the role of mtDNA and BER in aging brain and AD in order to design more effective preventive and therapeutic strategies.

Indexed as

DNA DamageDNA RepairAgingAlzheimer DiseaseAnimalsBrainDNA, MitochondrialHumansMitochondriaOxidation-ReductionOxidative StressReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID23216311
PMCPMC3671662

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.