ArticleNeuropsychiatric disease and treatment2020
Phosphorylation of Tau and α-Synuclein Induced Neurodegeneration in MPTP Mouse Model of Parkinson's Disease.
Article in Neuropsychiatric disease and treatment, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 55 citations in OpenAlex.
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- Rodent models and accompanying in vitro strategies for studying the etiology and therapy of Parkinson's disease.Journal of Parkinson's disease · 2026Review
- Neuroprotective Potential of Synaptamide in MPTP-Induced Parkinson's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Expression of Axonal Transport Proteins in Dopaminergic Neurons of the Substantia Nigra in Mouse Models of Preclinical and Clinical Stages of Parkinson's Disease.International journal of molecular sciences · 2026Article
- The Influence of Gut Microbiome on Alpha-Synuclein Aggregation: Implications for Parkinson's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Brain Alterations Linked to the MPTP Mouse Model of Parkinson's Disease Uncovered by Diffusion Kurtosis Imaging and Magnetic Resonance Spectroscopy.CNS neuroscience & therapeutics · 2026Article
- Osmotin-derived 9-amino-acid peptide alleviates α-synuclein and MPTP-induced glial cell activation mediated neuroinflammation, protecting dopaminergic neurons in Parkinson's disease mice brain.Journal of biomedical science · 2026Article
- Bridging the gap in Parkinson's disease research: from general pathophysiology to advanced 3d cell culture models.Cell communication and signaling : CCS · 2025Review
- Strain-Distinct α-Synuclein and Tau Cross-Seeding Uncovered by Correlative Approach with Optical Photothermal Infrared Sub-Micron Imaging.Journal of the American Chemical Society · 2025Article
- TUDCA combined with Syndopa protects the midbrain and gut from MPTP toxicity in a Parkinson's disease mouse model: Immunohistochemical evidence.Biomolecules & biomedicine · 2025Article
- A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
- HucMSCs-Derived Extracellular Vesicles Deliver RPS27A Protein to Manipulate the MDM2-P53 Axis and Ameliorate Neurological Dysfunction in Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Article
- Posttranslational Modifications ofPharmacological reviews · 2024Review
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
- Nr1h4 and Thrb ameliorate ER stress and provide protection in the MPTP mouse model of Parkinson's.Life science alliance · 2024Article
- Cognitive dysfunction in animal models of human lewy-body dementia.Frontiers in aging neuroscience · 2024Review
- Animal models of Parkinson's disease: bridging the gap between disease hallmarks and research questions.Translational neurodegeneration · 2023Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeParkinson's disease (PD) is the second most common neurodegenerative disease. The α-Synuclein is a major component of Lewy bodies and Lewy neurites, the pathologic hallmark of PD. It is known that α-Synuclein is phosphorylated (p-α-Synuclein) in PD and tau-hyperphosphorylation (p-Tau) is also a pathologic feature of PD. However, the relationship between p-Synuclein and p-Tau in PD is not clear, in particular in the MPTP model of PD. The purpose of this study was to reveal their relationship in the mouse MPTP model.
methodsFirstly, the p-α-Synuclein, α-Synuclein, p-Tau and Tau protein levels were analyzed. Then, GSK3β activation was determined using immunoblot and immunohistochemical staining. Finally, the dopaminergic neurodegeneration was assessed using Tyrosine Hydroxylase (TH) staining and retrograde labeling and microglial marker were labeled. Microglial activation and nigrostriatal pathway degeneration were observed.
resultsThe results showed that p-α-Synuclein, α-Synuclein, p-Tau and Tau were upregulated in both hippocampus and substantia nigra of the PD mouse model. Furthermore, p-α-Synuclein and p-Tau were localized in the same regions of substantial nigra (SN) and dentate gyrus (DG) of hippocampus (Hippo). The activated form of GSK3β (phosphor GSK3β Y216) was increased in multiple brain areas. The GSK3β inhibitor AZD1080 injected in MPTP mice suppressed the expression of p-Tau and p-GSK3β and improved motor functions.
conclusionThese findings revealed that p-α-Synuclein and p-Tau proteins are key pathological events leading to neurodegeneration and motor dysfunctions in the mouse MPTP model of PD. Our data suggest that the interference with the GSK3β activity may be an effective approach for the treatment of PD.
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