ArticleNeurobiology of aging2015
Metabolomic analysis of exercise effects in the POLG mitochondrial DNA mutator mouse brain.
Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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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.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Maternal Exercise Rescues Embryonic Osteogenesis Impaired due to POLG Mutation Through a Potential Apelin-ATF4 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Accumulated mtDNA mutations are linked to specific impairments in NADH-linked respiration.iScience · 2026Article
- The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome.Science advances · 2026Article
- Ubiquitous Expression ofLife (Basel, Switzerland) · 2025Article
- Brain somatic mutations in Alzheimer's disease: linking genetic mosaicism to neurodegeneration.Molecular neurodegeneration · 2025Review
- Genome copy number predicts extreme evolutionary rate variation in plant mitochondrial DNA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Pathophysiology of Cerebellar Degeneration in Mitochondrial Disorders: Insights from theInternational journal of molecular sciences · 2023Article
- Effective differentiation of double negative thymocytes requires high fidelity replication of mitochondrial DNA in an age dependent manner.Frontiers in immunology · 2023Article
- Effects of high-intensity interval training with hyperbaric oxygen.Frontiers in physiology · 2022Article
- Unraveling Parkinson's Disease Neurodegeneration: Does Aging Hold the Clues?Journal of Parkinson's disease · 2022Review
- Multi-omics studies reveal ameliorating effects of physical exercise on neurodegenerative diseases.Frontiers in aging neuroscience · 2022Review
- Exercise-Induced Benefits for Alzheimer's Disease by Stimulating Mitophagy and Improving Mitochondrial Function.Frontiers in aging neuroscience · 2021Review
- Current progress in the therapeutic options for mitochondrial disorders.Physiological research · 2020Article
- Kynurenine pathway, NADExperimental gerontology · 2020Review
- Exercise Training and Neurodegeneration in Mitochondrial Disorders: Insights From the Harlequin Mouse.Frontiers in physiology · 2020Article
- Article
- Voluntary exercise normalizes the proteomic landscape in muscle and brain and improves the phenotype of progeroid mice.Aging cell · 2019Article
- Mitochondrial dynamics and transport in Alzheimer's disease.Molecular and cellular neurosciences · 2019Review
- Physical Exercise and Mitochondrial Disease: Insights From a Mouse Model.Frontiers in neurology · 2019Article
- Impact of exercise on oocyte quality in the POLG mitochondrial DNA mutator mouse.Reproduction (Cambridge, England) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondrial DNA (mtDNA) mutator mice express a mutated form of mtDNA polymerase gamma that results an accelerated accumulation of somatic mtDNA mutations in association with a premature aging phenotype. An exploratory metabolomic analysis of cortical metabolites in sedentary and exercised mtDNA mutator mice and wild-type littermate controls at 9-10 months of age was performed. Pathway analysis revealed deficits in the neurotransmitters acetylcholine, glutamate, and aspartate that were ameliorated by exercise. Nicotinamide adenine dinucleotide (NAD) depletion and evidence of increased poly(adenosine diphosphate-ribose) polymerase 1 (PARP1)activity were apparent in sedentary mtDNA mutator mouse cortex, along with deficits in carnitine metabolites and an upregulated antioxidant response that largely normalized with exercise. These data highlight specific pathways that are altered in the brain in association with an accelerated age-related accumulation of somatic mtDNA mutations. These results may have relevance to age-related neurodegenerative diseases associated with mitochondrial dysfunction, such as Alzheimer's disease and Parkinson's disease and provide insights into potential mechanisms of beneficial effects of exercise on brain function.
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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.