ReviewCNS neuroscience & therapeutics2014
The centrality of mitochondria in the pathogenesis and treatment of Parkinson's disease.
Review in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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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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Who cites it
50 citing papers in PubMed, 105 citations in OpenAlex.
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- Adenine Nucleotide Translocase 1 Promotes Functional Integrity of Mitochondria via Activating DDIT3-CytC Pathway and Intensifying Actin Filament Structures.Molecular neurobiology · 2025Article
- The Role of Mitochondrial Pyruvate Carrier in Neurological Disorders.Molecular neurobiology · 2025Review
- Insights into therapeutic approaches for the treatment of neurodegenerative diseases targeting metabolic syndrome.Molecular biology reports · 2025Review
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Causal association between phenylalanine and Parkinson's disease: a two-sample bidirectional mendelian randomization study.Frontiers in genetics · 2024Article
- Retinal Changes in Parkinson's Disease: A Non-invasive Biomarker for Early Diagnosis.Cellular and molecular neurobiology · 2023Review
- Influence of the Mediterranean Diet on Healthy Aging.International journal of molecular sciences · 2023Review
- Curcumin and N-Acetylcysteine Nanocarriers Alone or Combined with Deferoxamine Target the Mitochondria and Protect against Neurotoxicity and Oxidative Stress in a Co-Culture Model of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Article
- The mouse nicotinamide mononucleotide adenylyltransferase chaperones diverse pathological amyloid client proteins.The Journal of biological chemistry · 2022Article
- Gene Therapeutic Approaches for the Treatment of Mitochondrial Dysfunction in Parkinson's Disease.Genes · 2021Review
- A High-Throughput Chemical Screen in DJ-1β Mutant Flies Identifies Zaprinast as a Potential Parkinson's Disease Treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- IFN-β rescues neurodegeneration by regulating mitochondrial fission via STAT5, PGAM5, and Drp1.The EMBO journal · 2021Article
- Protective effects of Astragaloside IV against oxidative injury and apoptosis in cultured astrocytes by regulating Nrf2/JNK signaling.Experimental brain research · 2021Article
- Docosahexaenoic and Arachidonic Acids as Neuroprotective Nutrients throughout the Life Cycle.Nutrients · 2021Review
- Redox Homeostasis and Prospects for Therapeutic Targeting in Neurodegenerative Disorders.Oxidative medicine and cellular longevity · 2021Review
- N-Acetylcysteine Nanocarriers Protect against Oxidative Stress in a Cellular Model of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2020Article
- A Mouse Model of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-Induced Parkinson Disease Shows that 2-Aminoquinoline Targets JNK Phosphorylation.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Bu-Yin-Qian-Zheng Formula Ameliorates MPPFrontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is an incurable neurodegenerative disorder leading to progressive motor impairment and for which there is no cure. From the first postmortem account describing a lack of mitochondrial complex I in the substantia nigra of PD sufferers, the direct association between mitochondrial dysfunction and death of dopaminergic neurons has ever since been consistently corroborated. In this review, we outline common pathways shared by both sporadic and familial PD that remarkably and consistently converge at the level of mitochondrial integrity. Furthermore, such knowledge has incontrovertibly established mitochondria as a valid therapeutic target in neurodegeneration. We discuss several mitochondria-directed therapies that promote the preservation, rescue, or restoration of dopaminergic neurons and which have been identified in the laboratory and in preclinical studies. Some of these have progressed to clinical trials, albeit the identification of an unequivocal disease-modifying neurotherapeutic is still elusive. The challenge is therefore to improve further, not least by more research on the molecular mechanisms and pathophysiological consequences of mitochondrial dysfunction in PD.
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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.