ReviewInternational journal of molecular sciences2025
Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson's Disease.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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.
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Who cites it
24 citing papers in PubMed.
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Moringa oleifera Lam. Seed Lectin (WSMoL) Attenuates Parkinsonian Symptoms in Mice via Anti-Inflammatory, Antioxidant, and Neurotransmitter-Modulating Effects.Chemistry & biodiversity · 2026Article
- Parkinson's Disease: Pathophysiology, Treatment Strategies, Wellness Approaches, and Obstacles/Paths Forward.NeuroSci · 2026Review
- The role of mitochondrial Na⁺/Ca²⁺ exchanger in brain cell aging.Journal of bioenergetics and biomembranes · 2026Review
- Reimagining the contribution of iron in Parkinson's disease.Neurobiology of disease · 2026Review
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Mitochondrial Dysfunction as a Driver of Neurodegeneration in Parkinson's and Huntington's Disease: Molecular Insights and Emerging Interventions.Molecular neurobiology · 2026Review
- Bibliometric analysis of nanomaterials in the diagnosis and treatment of neurological and psychiatric disorders (1997-2025): trends and future directions.Journal of nanobiotechnology · 2026Review
- Investigation of the Effects of Saffron on Neuroprotection and Circadian Rhythm in anPharmaceuticals (Basel, Switzerland) · 2026Article
- Photonic and nanomaterial-driven optical biosensing strategies for Parkinson's disease.Mikrochimica acta · 2026Review
- Review
- Mitochondrial Proteins in Putative Neuron-Derived Plasma Exosomes Are Altered in Parkinson's Disease: An Exploratory Study.Molecular neurobiology · 2026Article
- Mitoepigenetic Alterations in Early-Onset Parkinson's Disease.International journal of molecular sciences · 2026Article
- HUWE1 regulates mitophagy to protect dopaminergic neurons from 6-OHDA- and MPP⁺-induced neurotoxicity.Cell biology and toxicology · 2026Article
- Exploring the Role of Food and Food-Related Compounds in Parkinson's Disease.Foods (Basel, Switzerland) · 2026Review
- The Vesicular Glutamate Transporter Modulates Sex and Region-Specific Differences in Dopaminergic Neuron α-Synuclein Toxicity by Modifying Cytosolic Dopamine Levels.bioRxiv : the preprint server for biology · 2026Article
- The role of energy deficit in autophagy failure in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- Identification of Gene Signatures and Molecular Mechanisms for Diagnosing Parkinson's Disease and Nonalcoholic Fatty Liver Disease Using Machine Learning.Parkinson's disease · 2026Article
- Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.Frontiers in pharmacology · 2026Review
- Expanding the Arsenal of Nanocarriers Against Parkinson Disease: Success so Far Roads Ahead.AAPS PharmSciTech · 2025Review
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.
Funding
Abstract
Mitochondrial dysfunction is a hallmark of Parkinson's disease (PD) pathogenesis, contributing to increased oxidative stress and impaired endo-lysosomal-proteasome system efficiency underlying neuronal injury. Genetic studies have identified 19 monogenic mutations-accounting for ~10% of PD cases-that affect mitochondrial function and are associated with early- or late-onset PD. Early-onset forms typically involve genes encoding proteins essential for mitochondrial quality control, including mitophagy and structural maintenance, while late-onset mutations impair mitochondrial dynamics, bioenergetics, and trafficking. Atypical juvenile genetic syndromes also exhibit mitochondrial abnormalities. In idiopathic PD, environmental neurotoxins such as pesticides and MPTP act as mitochondrial inhibitors, disrupting complex I activity and increasing reactive oxygen species. These converging pathways underscore mitochondria as a central node in PD pathology. This review explores the overlapping and distinct mitochondrial mechanisms in genetic and non-genetic PD, emphasizing their role in neuronal vulnerability. Targeting mitochondrial dysfunction finally offers a promising therapeutic avenue to slow or modify disease progression by intervening at a key point of neurodegenerative convergence.
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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.