SynthesisNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2021
A systematic review of molecular approaches that link mitochondrial dysfunction and neuroinflammation in Parkinson's disease.
Synthesis in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Chronic Paraquat Neurotoxicity and Dopaminergic Degeneration: A Mechanistic Review.Chemistry & biodiversity · 2026Review
- Targeting mtDNA to Modulate Mitochondrial Dysfunction in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Metabolic Remodeling of the Parkinson's Disease Frontal Cortex Revealed by LC-MS/MS Metabolomics.Biomolecules · 2026Article
- Progress in the study of ion channel function, mechanisms, and mathematical modeling in Parkinson's disease.iScience · 2026Review
- Xmu-mp-1 attenuates streptozotocin-induced neurotoxicity in SH-SY5Y cells: potential role of Hippo pathway modulation.Molecular biology reports · 2026Article
- Micro-nanoplastics and Parkinson's disease: evidence and perspectives.NPJ Parkinson's disease · 2026Review
- Review
- Neuroprotective role of bilirubin in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- Lupeol restores dopaminergic function by suppressing glial activation in a Parkinson's disease mouse model.Frontiers in immunology · 2026Article
- A recent review on ginseng's effects on neurodegenerative diseases: active ingredients, mechanisms of action, applications, and delivery strategies.Frontiers in nutrition · 2026Review
- Targeting TMEM175 in Lysosomal Physiology and Human Diseases.Current stem cell research & therapy · 2026Review
- An update on the involvement of inflammatory mediators in Parkinson's disease pathogenesis.Archives of toxicology · 2025Review
- The Neuroprotective Effects of Agmatine on Parkinson's Disease: Focus on Oxidative Stress, Inflammation and Molecular Mechanisms.Inflammation · 2025Review
- Neurocognitive correlates of cerebral mitochondrial function and energy metabolism using phosphorus magnetic resonance spectroscopy in older adults.GeroScience · 2025Article
- VDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration.Biomolecules · 2024Review
- Association Between Common Variants in theInternational journal of molecular sciences · 2024Article
- Astrocyte-derived apolipoprotein D is required for neuronal survival in Parkinson's disease.NPJ Parkinson's disease · 2024Article
- Multiomics of parkinsonism cynomolgus monkeys highlights significance of metabolites in interaction between host and microbiota.NPJ biofilms and microbiomes · 2024Article
- Frontal-temporal regional differences in brain energy metabolism and mitochondrial function usingGeroScience · 2024Article
- Integration of National Health Insurance claims data and animal models reveals fexofenadine as a promising repurposed drug for Parkinson's disease.Journal of neuroinflammation · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder that affects 1% of the population worldwide. Etiology of PD is likely to be multi-factorial such as protein misfolding, mitochondrial dysfunction, oxidative stress, and neuroinflammation that contributes to the pathology of Parkinson's disease (PD), numerous studies have shown that mitochondrial dysfunction may play a key role in the dopaminergic neuronal loss. In multiple ways, the two most important are the activation of neuroinflammation and mitochondrial dysfunction, while mitochondrial dysfunction could cause neuroinflammation and vice versa. Thus, the mitochondrial proteins are the highly promising target for the development of PD. However, the limited amount of dopaminergic neurons prevented the detailed investigation of Parkinson's disease with regard to mitochondrial dysfunction. Both genetic and environmental factors are also associated with mitochondrial dysfunction and PD pathogenesis. The induction of PD by neurotoxins that inhibit mitochondrial complex I provide direct evidence linking mitochondrial dysfunction to PD. A decrease of mitochondrial complex I activity is observed in PD brain and in neurotoxin- or genetic factor-induced in vitro and in vivo models. Moreover, PINK1, Parkin, DJ-1 and LRRK2 mitochondrial PD gene products have important roles in mitophagy, a cellular process that clear damaged mitochondria. This review paper would discuss the evidence for the mitochondrial dysfunction and neuroinflammation 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.