ReviewJournal of Parkinson's disease2025
Aging, cellular senescence and Parkinson's disease.
Review in Journal of Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled 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.
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, 1 synthesis or guideline pooled it.
- Levodopa and Plant-Derived Bioactive Compounds in Parkinson's Disease: Mechanisms, Efficacy, and Future Perspectives.CNS neuroscience & therapeutics · 2025Pooled it
- Microenvironmental barriers to healing in osteoradionecrosis and opportunities for regenerative intervention.Bioactive materials · 2027Review
- Article
- Traditional Chinese Medicine Formulas in Delaying Aging: From Theoretical Foundations to Molecular Mechanisms and Translational Perspectives.Journal of cellular and molecular medicine · 2026Review
- Preliminary insights into whole-blood mitochondrial DNA copy number and telomere length in Parkinson's disease and multiple system atrophy.Journal of neurology · 2026Article
- Mitochondrial transplantation reverses the senescence phenotype of SH-SY5Y cells.Molecular therapy. Advances · 2026Article
- Rethinking Senescence Hallmarks in the Brain: Lessons From Peripheral Tissues and Challenges in Defining Neuronal Senescence.Aging cell · 2026Review
- Obesity accelerates aging: Mechanisms and therapeutic implications.Genes & diseases · 2026Review
- Research progress of traditional Chinese medicine interventions for aging-related nervous system diseases.Biogerontology · 2026Review
- Targeting the FOXO4-p53 axis by retro-inverso peptide senolytic agents: a pharmacological strategy to mitigate brain aging and cognitive decline.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Rethinking our strategies to develop disease-modifying therapies for Parkinson's: Time for combination therapies?Journal of Parkinson's disease · 2026Article
- Early-Life Rotenone Exposure Enhances Nigrostriatal Vulnerability and Parkinsonian Neurodegeneration in Aging Rats.Toxics · 2026Article
- MicroRNA-Mediated Regulation of Brain Aging Hallmarks: Implications for Neurodegeneration and Neural Recovery.Brain and behavior · 2026Review
- Frailty index predicts the risk of 17 health outcomes in distinct ways: prospective findings from the Moli-sani Study.Age and ageing · 2026Article
- Cellular Senescence in Neurodegeneration: From Cell Types to Therapeutic Opportunities.Biomedicines · 2026Review
- Multimodal Cancer Therapy and Accelerated Brain Aging: Mechanisms, Biomarkers, and Clinical Consequences.Current oncology (Toronto, Ont.) · 2026Review
- Emerging Roles, Mechanisms, and Therapeutic Potential of Thyroid Hormones in Neurodegenerative Diseases: A Review.Brain sciences · 2026Review
- Association Between Relative Fat Mass and Parkinson's Disease in American Adults: A Large Cross-Sectional Study From NHANES.Parkinson's disease · 2026Article
- Cuproptosis-associated genesFrontiers in immunology · 2026Article
- Triglyceride-glucose index is associated with cerebral small vessel disease-related motor impairment in Parkinson's disease: a mediation analysis.Frontiers in aging neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is the most common neurodegenerative movement disorder, affecting 1-2% of people over age 65. The risk of developing PD dramatically increases with advanced age, indicating that aging is likely a driving factor in PD neuropathogenesis. Several age-associated biological changes are also hallmarks of PD neuropathology, including mitochondrial dysfunction, oxidative stress, and neuroinflammation. Accumulation of senescent cells is an important feature of aging that contributes to age-related diseases. How age-related cellular senescence affects brain health and whether this phenomenon contributes to neuropathogenesis in PD is not yet fully understood. In this review, we highlight hallmarks of aging, including mitochondrial dysfunction, loss of proteostasis, genomic instability and telomere attrition in relation to well established PD neuropathological pathways. We then discuss the hallmarks of cellular senescence in the context of neuroscience and review studies that directly examine cellular senescence in PD. Studying senescence in PD presents challenges and holds promise for advancing our understanding of disease mechanisms, which could contribute to the development of effective disease-modifying therapeutics. Targeting senescent cells or modulating the senescence-associated secretory phenotype (SASP) in PD requires a comprehensive understanding of the complex relationship between PD pathogenesis and cellular senescence.
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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.