ArticleInternational journal of molecular sciences2018
Dopamine Transporter/α-Synuclein Complexes Are Altered in the Post Mortem Caudate Putamen of Parkinson's Disease: An In Situ Proximity Ligation Assay Study.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Oleuropein regulates neuronal survival and Histone acetylation in Parkinson's disease: cellular and epigenetic insights.Metabolic brain disease · 2026Article
- Seeing Invisible Oligomers: Rethinking α-Synuclein Pathology Through Proximity Ligation Assay.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- 14-3-3σ up-regulation in the temporal cortex associates with tau pathology and reactive astroglia in Lewy body disorders.Brain pathology (Zurich, Switzerland) · 2026Article
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- Brain virome dysbiosis in Parkinson's disease and multiple system atrophy.Frontiers in microbiology · 2025Article
- Advancement in human neuroimaging based on proximity ligation assay in brain disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Striatal dopamine neurotransmission is altered in age- and region-specific manner in a Parkinson's disease transgenic mouse.Scientific reports · 2024Article
- Synuclein Proteins in MPTP-Induced Death of Substantia Nigra Pars Compacta Dopaminergic Neurons.Biomedicines · 2022Review
- Dopaminergic Positron Emission Tomography Imaging in the Alpha-Synuclein Preformed Fibril Model Reveals Similarities to Early Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Methylphenidate Analogues as a New Class of Potential Disease-Modifying Agents for Parkinson's Disease: Evidence from Cell Models and Alpha-Synuclein Transgenic Mice.Pharmaceutics · 2022Article
- Alpha-Synuclein is Involved in DYT1 Dystonia Striatal Synaptic Dysfunction.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Synapsin III gene silencing redeems alpha-synuclein transgenic mice from Parkinson's disease-like phenotype.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Inhibition of LRRK2 kinase activity promotes anterograde axonal transport and presynaptic targeting of α-synuclein.Acta neuropathologica communications · 2021Article
- The Association between α-Synuclein and α-Tubulin in Brain Synapses.International journal of molecular sciences · 2021Article
- Integrating the Roles of Midbrain Dopamine Circuits in Behavior and Neuropsychiatric Disease.Biomedicines · 2021Review
- Experimental Dopamine Reuptake Inhibitors in Parkinson's Disease: A Review of the Evidence.Journal of experimental pharmacology · 2021Review
- Article
- Intrastriatal alpha-synuclein fibrils in monkeys: spreading, imaging and neuropathological changes.Brain : a journal of neurology · 2019Article
- Revealing Adenosine AInternational journal of molecular sciences · 2019Article
- Is Braak staging valid for all types of Parkinson's disease?Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
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5 authors.
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Abstract
Parkinson's disease (PD) is characterized by the degeneration of the dopaminergic nigrostriatal neurons and the presence of Lewy bodies (LB) and Lewy neurites (LN) mainly composed of α-synuclein. By using the in situ proximity ligation assay (PLA), which allows for the visualization of protein-protein interactions in tissues to detect dopamine transporter (DAT)/α-synuclein complexes, we previously described that these are markedly redistributed in the striatum of human α-synuclein transgenic mice at the phenotypic stage, showing dopamine (DA) release impairment without a DAT drop and motor symptoms. Here, we used the in situ PLA to investigate DAT/α-synuclein complexes in the caudate putamen of PD patients and age-matched controls. They were found to be redistributed and showed an increased size in PD patients, where we observed several neuropil-like and neuritic-like PLA-positive structures. In the PD brains, DAT immunolabeling showed a pattern similar to that of in situ PLA in areas with abundant α-synuclein neuropathology. This notwithstanding, the in situ PLA signal was only partially retracing DAT or α-synuclein immunolabeling, suggesting that a large amount of complexes may have been lost along with the degeneration process. These findings reveal a DAT/α-synuclein neuropathological signature in PD and hint that synaptic alterations involving striatal DAT may derive from α-synuclein aggregation.
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