ReviewGenes2018
Brain Mitochondria, Aging, and Parkinson's Disease.
Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 82 citations in OpenAlex.
- The role of gut microbiota-mitochondria crosstalk in neurodegeneration: Underlying mechanisms and potential therapies.Neural regeneration research · 2026Article
- α-tocopherol alleviates ketamine toxicity in rat brain neurons.BMC pharmacology & toxicology · 2026Article
- α-Synuclein Degradation in Brain Pericytes Is Mediated via Akt, ERK, and p38 MAPK Signaling Pathways.International journal of molecular sciences · 2025Article
- Predictors associated with the rate of progression of nigrostriatal degeneration in Parkinson's disease.Journal of neurology · 2024Article
- Mitophagy and cGAS-STING crosstalk in neuroinflammation.Acta pharmaceutica Sinica. B · 2024Review
- Mitochondrial metabolism in neural stem cells and implications for neurodevelopmental and neurodegenerative diseases.Journal of translational medicine · 2024Review
- High-Resolution Respirometry for Mitochondrial Function in Rodent Brain.Methods in molecular biology (Clifton, N.J.) · 2024Article
- YKL-40 and the Cellular Metabolic Profile in Parkinson's Disease.International journal of molecular sciences · 2023Article
- JAC4 Alleviates Rotenone-Induced Parkinson's Disease through the Inactivation of the NLRP3 Signal Pathway.Antioxidants (Basel, Switzerland) · 2023Article
- Escalating Bi-Directional Feedback Loops between Proinflammatory Microglia and Mitochondria in Ageing and Post-Diagnosis of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial Modulators: The Defender.Biomolecules · 2023Review
- Mitochondrial Interaction with Serotonin in Neurobiology and Its Implication in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Review
- Paving the way while playing catch up: mitochondrial genetics in African ancestry primary open-angle glaucoma.Frontiers in ophthalmology · 2023Article
- Pathological and Therapeutic Advances in Parkinson's Disease: Mitochondria in the Interplay.Journal of Alzheimer's disease : JAD · 2023Review
- Oxidative stress in the brain and retina after traumatic injury.Frontiers in neuroscience · 2023Review
- Signatures of adaptive evolution in platyrrhine primate genomes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Exploring the Role of Ubiquitin-Proteasome System in Parkinson's Disease.Molecular neurobiology · 2022Review
- From the Structural and (Dys)Function of ATP Synthase to Deficiency in Age-Related Diseases.Life (Basel, Switzerland) · 2022Review
- Normal Aging Induces Changes in the Brain and Neurodegeneration Progress: Review of the Structural, Biochemical, Metabolic, Cellular, and Molecular Changes.Frontiers in aging neuroscience · 2022Review
- Mitochondrial support and local translation of mitochondrial proteins in synaptic plasticity and function.Histology and histopathology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This paper reconsiders the role of mitochondria in aging and in Parkinson's Disease (PD). The most important risk factor for PD is aging. Alterations in mitochondrial activity are typical of aging. Mitochondrial aging is characterized by decreased oxidative phosphorylation, proteasome activity decrease, altered autophagy, and mitochondrial dysfunction. Beyond declined oxidative phosphorylation, mitochondrial dysfunction consists of a decline of beta-oxidation as well as of the Krebs cycle. Not inherited mitochondrial DNA (mtDNA) mutations are acquired over time and parallel the decrease in oxidative phosphorylation. Many of these mitochondrial alterations are also found in the PD brain specifically in the substantia nigra (SN). mtDNA deletions and development of respiratory chain deficiency in SN neurons of aged individuals as well as of individuals with PD converge towards a shared pathway, which leads to neuronal dysfunction and death. Finally, several nuclear genes that are mutated in hereditary PD are usually implicated in mitochondrial functioning to a various extent and their mutation may cause mitochondrial impairment. In conclusion, a tight link exists between mitochondria, aging, and PD.
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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.