ReviewDNA repair2008
Mitochondrial DNA, base excision repair and neurodegeneration.
Review in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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.
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.
Who cites it
50 citing papers in PubMed, 98 citations in OpenAlex.
- Exercise alone or combined with functional foods in aging and age-related diseases: targeting DNA damage, repair pathways, and genome integrity.Frontiers in aging neuroscience · 2026Review
- Natural Product Treatment for Metabolic Dysfunction-Associated Steatotic Liver Disease: Targeted Mitochondrial Quality Control.Drug design, development and therapy · 2026Review
- Biallelic variants in theMolecular genetics and metabolism reports · 2024Article
- The Mitochondrial Connection: The Nek Kinases' New Functional Axis in Mitochondrial Homeostasis.Cells · 2024Review
- Metabolic and proteostatic differences in quiescent and active neural stem cells.Neural regeneration research · 2024Review
- G-quadruplexes and associated proteins in aging and Alzheimer's disease.Frontiers in aging · 2023Review
- Simultaneous Short- and Long-Patch Base Excision Repair (BER) Assay in Live Mammalian Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Activated or Impaired: An Overview of DNA Repair in Neurodegenerative Diseases.Aging and disease · 2022Article
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- NEK5 interacts with LonP1 and its kinase activity is essential for the regulation of mitochondrial functions and mtDNA maintenance.FEBS open bio · 2021Article
- The role of exercise in brain DNA damage.Neural regeneration research · 2020Review
- The Similarities between Human Mitochondria and Bacteria in the Context of Structure, Genome, and Base Excision Repair System.Molecules (Basel, Switzerland) · 2020Review
- DNA damage response and repair pathway modulation by non-histone protein methylation: implications in neurodegeneration.Journal of cell communication and signaling · 2020Review
- SCAN1-TDP1 trapping on mitochondrial DNA promotes mitochondrial dysfunction and mitophagy.Science advances · 2019Article
- Review
- Biothiols and oxidative stress markers and polymorphisms ofOncotarget · 2018Article
- Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases.Nature reviews. Molecular cell biology · 2017Review
- Naked mole-rats maintain healthy skeletal muscle and Complex IV mitochondrial enzyme function into old age.Aging · 2016Article
- Oxidative DNA damage stalls the human mitochondrial replisome.Scientific reports · 2016Article
- DNA Damage, DNA Repair, Aging, and Neurodegeneration.Cold Spring Harbor perspectives in medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Neurodegeneration is a growing public health concern because of the rapid increase in median and maximum life expectancy in the developed world. Mitochondrial dysfunction seems to play a critical role in neurodegeneration, likely owing to the high energy demand of the central nervous system and its sole reliance on oxidative metabolism for energy production. Loss of mitochondrial function has been clearly demonstrated in several neuropathologies, most notably those associated with age, like Alzheimer's, Parkinson's and Huntington's diseases. Among the common features observed in such conditions is the accumulation of oxidative DNA damage, in particular in the mitochondrial DNA, suggesting that mitochondrial DNA instability may play a causative role in the development of these diseases. In this review we examine the evidence for the accumulation of oxidative DNA damage in mitochondria, and its relationship with loss of mitochondrial function and cell death in neural tissues. Oxidative DNA damage is repaired mainly by the base excision repair pathway. Thus, we review the molecular events and enzymes involved in base excision repair in mitochondria, and explore the possible role of alterations in mitochondrial base excision repair activities in premature aging and age-associated neurodegenerative diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.