ArticleMolecular neurodegeneration2016
Pioglitazone ameliorates the phenotype of a novel Parkinson's disease mouse model by reducing neuroinflammation.
Article in Molecular neurodegeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses that pooled it.
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Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- Does glitazone treatment have a role on the prevention of Parkinson's disease in adult diabetic population? A systematic review.Metabolic brain disease · 2020Pooled it
- Decreased risk of Parkinson's disease in diabetic patients with thiazolidinediones therapy: An exploratory meta-analysis.PloS one · 2019Pooled it
- Mitochondrial transplantation reverses the senescence phenotype of SH-SY5Y cells.Molecular therapy. Advances · 2026Article
- PPARγ-Dependent Pioglitazone Treatment Suppresses Neuroinflammation and Improves Cognition in Sepsis-Associated Encephalopathy in Mice.CNS neuroscience & therapeutics · 2026Article
- Repurposing Antidiabetic Medications for Parkinson's Disease: Focus on Biomarker Strategies for Disease Modification.International journal of molecular sciences · 2026Review
- Pioglitazone Ameliorates Mitochondrial Oxidative Stress and Inflammation via AMPK-Dependent Inhibition of Mitochondrial Fission in Leigh Syndrome.Cell proliferation · 2026Article
- Biomimetic nanodelivery system with simultaneous blood-brain barrier-crossing and neuroprotective abilities for anti-parkinsonian therapy.Chinese medicine · 2025Article
- Pioglitazone Modulates Microglia M1/M2 Polarization Through PPAR-γ Pathway and Exerts Neuroprotective Effects in Experimental Subarachnoid Hemorrhage.Molecular neurobiology · 2025Article
- Adolescent mice exposed to TBI developed PD-like pathology in middle age.Translational psychiatry · 2025Article
- Neuroimmune crosstalk in chronic neuroinflammation: microglial interactions and immune modulation.Frontiers in cellular neuroscience · 2025Review
- Comparative Analysis of Pioglitazone and Tirzepatide on Body Weight, Glucose Levels, Neuroinflammation, and Oxidative Stress in Diabetic Rats.Drug design, development and therapy · 2025Article
- Cohort-specific boolean models highlight different regulatory modules during Parkinson's disease progression.iScience · 2024Article
- Cannabidiol ameliorates mitochondrial disease via PPARγ activation in preclinical models.Nature communications · 2024Article
- The Contribution of Type 2 Diabetes to Parkinson's Disease Aetiology.International journal of molecular sciences · 2024Review
- Mitochondrial dysfunction in Parkinson's disease - a key disease hallmark with therapeutic potential.Molecular neurodegeneration · 2023Review
- Metabolic dysfunctions in the intranigral rotenone model of Parkinson's disease.Experimental brain research · 2023Article
- Rosiglitazone Mitigates Dexamethasone-Induced Depression in Mice via Modulating Brain Glucose Metabolism and AMPK/mTOR Signaling Pathway.Biomedicines · 2023Article
- The Therapeutic Potential of Mitochondria Transplantation Therapy in Neurodegenerative and Neurovascular Disorders.Current neuropharmacology · 2023Review
- Pioglitazone in spontaneous subarachnoid hemorrhage: study protocol of a multicenter, double-blind, randomized trial (PSSH).Frontiers in pharmacology · 2023Article
- Association between Parkinson's Disease and Diabetes Mellitus: From Epidemiology, Pathophysiology and Prevention to Treatment.Aging and disease · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundParkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms. The cause of the motor symptoms is the loss of dopaminergic neurons in the substantia nigra with consequent depletion of dopamine in the striatum. Although the etiology of PD is unknown, mitochondrial dysfunctions, including cytochrome c oxidase (Complex IV) impairment in dopaminergic neurons, have been associated with the disease's pathophysiology. In order to analyze the role of Complex IV in PD, we knocked out Cox10 (essential for the maturation of COXI, a catalytic subunit of Complex IV) in dopaminergic neurons. We also tested whether the resulting phenotype was improved by stimulating the PPAR-γ pathway.
resultsCox10/DAT-cre mice showed decreased numbers of TH+ and DAT+ cells in the substantia nigra, early striatal dopamine depletion, motor defects reversible with L-DOPA treatment and hypersensitivity to L-DOPA with hyperkinetic behavior. We found that chronic pioglitazone (PPAR-γ agonist) treatment ameliorated the motor phenotype in Cox10/DAT-cre mice. Although neither mitochondrial function nor the number of dopaminergic neurons was improved, neuroinflammation in the midbrain and the striatum was decreased.
conclusionsBy triggering a mitochondrial Complex IV defect in dopaminergic neurons, we created a new mouse model resembling the late stages of PD with massive degeneration of dopaminergic neurons and striatal dopamine depletion. The motor phenotypes were improved by Pioglitazone treatment, suggesting that targetable secondary pathways can influence the development of certain forms of PD.
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