ReviewFrontiers in neuroscience2019
Intracellular and Intercellular Mitochondrial Dynamics in Parkinson's Disease.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05855577 (-Clinical Efficacy of Pharmacological Treatments Targeting Energy Metabolism, Evaluated by Gait Analysis, on Motor Function in Parkinson's Disease Patients), which is not on this map. Cited by 45 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.
-Clinical Efficacy of Pharmacological Treatments Targeting Energy Metabolism, Evaluated by Gait Analysis, on Motor Function in Parkinson's Disease Patients
Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
- Phytogenic Nanoparticles for Parkinson's Disease Therapy: Mechanistic Insights, Brain-Targeted Delivery and Neuroprotective Potential.Molecular neurobiology · 2026Review
- Tissue Effects of the Mitochondrial Division Inhibitor Mdivi-1 on the Substantia Nigra in a Laboratory Model of Dopaminergic System Damage.International journal of molecular sciences · 2026Article
- Unraveling Parkinson's disease: The mystery of mitochondria and the role of aging.Genes & diseases · 2026Review
- Human dental pulp stem cell-derived mitochondria restore mitochondrial function and promote neuroregeneration in a cellular model of Parkinson's disease.Stem cell research & therapy · 2025Article
- Alpha-synuclein interacts with regulators of ATP homeostasis in mitochondria.Nature communications · 2025Article
- Mitochondrial Dynamics in Brain Cells During Normal and Pathological Aging.International journal of molecular sciences · 2024Review
- Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.International journal of molecular sciences · 2024Review
- Human tripartite cortical network model for temporal assessment of alpha-synuclein aggregation and propagation in Parkinson's Disease.NPJ Parkinson's disease · 2024Article
- Disease Mechanisms of Multiple System Atrophy: What a Parallel Between the Form of Pasta and the Alpha-Synuclein Assemblies Involved in MSA and PD Tells Us.Cerebellum (London, England) · 2024Review
- YKL-40 and the Cellular Metabolic Profile in Parkinson's Disease.International journal of molecular sciences · 2023Article
- Article
- Rescuers from the Other Shore: Intercellular Mitochondrial Transfer and Its Implications in Central Nervous System Injury and Diseases.Cellular and molecular neurobiology · 2023Review
- Mitochondrial Dysfunction and Parkinson's Disease: Pathogenesis and Therapeutic Strategies.Neurochemical research · 2023Review
- Understanding the Involvement of microRNAs in Mitochondrial Dysfunction and Their Role as Potential Biomarkers and Therapeutic Targets in Parkinson's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Mitochondrial transport in neurons and evidence for its involvement in acute neurological disorders.Frontiers in neuroscience · 2023Review
- The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation.Frontiers in molecular neuroscience · 2023Review
- Impaired migratory phenotype of CD4NPJ Parkinson's disease · 2022Article
- Genetic Study of Early Onset Parkinson's Disease in Cyprus.International journal of molecular sciences · 2022Article
- Review
- The Hidden Notes of Redox Balance in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The appearance of alpha-synuclein-positive inclusion bodies (Lewy bodies) and the loss of catecholaminergic neurons are the primary pathological hallmarks of Parkinson's disease (PD). However, the dysfunction of mitochondria has long been recognized as a key component in the progression of the disease. Dysfunctional mitochondria can in turn lead to dysregulation of calcium homeostasis and, especially in dopaminergic neurons, raised mean intracellular calcium concentration. As calcium binding to alpha-synuclein is one of the important triggers of alpha-synuclein aggregation, mitochondrial dysfunction will promote inclusion body formation and disease progression. Increased reactive oxygen species (ROS) resulting from inefficiencies in the electron transport chain also contribute to the formation of alpha-synuclein aggregates and neuronal loss. Recent studies have also highlighted defects in mitochondrial clearance that lead to the accumulation of depolarized mitochondria. Transaxonal and intracytoplasmic translocation of mitochondria along the microtubule cytoskeleton may also be affected in diseased neurons. Furthermore, nanotube-mediated intercellular transfer of mitochondria has recently been reported between different cell types and may have relevance to the spread of PD pathology between adjacent brain regions. In the current review, the contributions of both intracellular and intercellular mitochondrial dynamics to the etiology of PD will be discussed.
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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.