ArticleTranslational neurodegeneration2018
Age-dependent alpha-synuclein accumulation and aggregation in the colon of a transgenic mouse model of Parkinson's disease.
Article in Translational neurodegeneration, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 44 citations in OpenAlex.
- Gut-brain axis dysregulation in Parkinson's disease: Mechanisms linking microbiota to neuroinflammation and α-synuclein pathology.Journal of pharmaceutical analysis · 2026Review
- Bidirectional communication between the gut microbiota and the central nervous system.Neural regeneration research · 2026Article
- The α-Synuclein Seeding Amplification Assay for Parkinson's Disease.International journal of molecular sciences · 2025Review
- Advances in autonomic dysfunction research in Parkinson's disease.Frontiers in aging neuroscience · 2025Review
- Posttranslational Modifications ofPharmacological reviews · 2024Review
- Overlaps and divergences between tauopathies and synucleinopathies: a duet of neurodegeneration.Translational neurodegeneration · 2024Review
- Gut-Brain Axis Deregulation and Its Possible Contribution to Neurodegenerative Disorders.Neurotoxicity research · 2023Review
- Impact of Microbiome-Brain Communication on Neuroinflammation and Neurodegeneration.International journal of molecular sciences · 2023Review
- Long-term hyperglycemia aggravates α-synuclein aggregation and dopaminergic neuronal loss in a Parkinson's disease mouse model.Translational neurodegeneration · 2022Article
- Gut-Derived Sterile Inflammation and Parkinson's Disease.Frontiers in neurology · 2022Review
- The Pathological Mechanism Between the Intestine and Brain in the Early Stage of Parkinson's Disease.Frontiers in aging neuroscience · 2022Review
- Epigenetic inactivation of the autophagy-lysosomal system in appendix in Parkinson's disease.Nature communications · 2021Article
- Enteric glial biology, intercellular signalling and roles in gastrointestinal disease.Nature reviews. Gastroenterology & hepatology · 2021Review
- Ageing promotes pathological alpha-synuclein propagation and autonomic dysfunction in wild-type rats.Brain : a journal of neurology · 2021Article
- Differential seeding and propagating efficiency of α-synuclein strains generated in different conditions.Translational neurodegeneration · 2021Article
- Parkinson mice show functional and molecular changes in the gut long before motoric disease onset.Molecular neurodegeneration · 2021Article
- Alpha Synuclein Connects the Gut-Brain Axis in Parkinson's Disease Patients - A View on Clinical Aspects, Cellular Pathology and Analytical Methodology.Frontiers in cell and developmental biology · 2020Review
- Cynomolgus Monkeys With Spontaneous Type-2-Diabetes-Mellitus-Like Pathology Develop Alpha-Synuclein Alterations Reminiscent of Prodromal Parkinson's Disease and Related Diseases.Frontiers in neuroscience · 2020Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParkinson's disease (PD) is one of the most common neurodegenerative diseases, neuropathologically characterized by misfolded protein aggregation, called Lewy bodies and Lewy neurites. PD is a slow-progressive disease with colonic dysfunction appearing in the prodromal stage and lasting throughout the course of the disease.
methodsIn order to study PD pathology in the colon, we examined the age-dependent morphological and pathological changes in the colon of a PD mouse model expressing human wildtype α-synuclein (α-syn) fused with the green fluorescent protein (GFP), under the endogenous mouse α-syn promoter.
resultsWe observed an age-dependent progressive expression and accumulation of α-syn-GFP in the enteric neurons of Meissner's (submucosal) and Auerbach's (myenteric) plexuses of the colon. Additionally, the phosphorylation of α-syn at serine 129 also increased with age and the aggregation of α-syn-GFP coincided with the appearance of motor deficits at 9 months of age. Furthermore, α-syn (-GFP) distinctly co-localized with different subtypes of neurons, as identified by immunohistochemical labeling of vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (nNOS), and calretinin.
conclusionsOur results show the development of α-syn pathology in the enteric neurons of the colon in a PD mouse model, which coincide with the appearance of motor deficits. Our mouse model possesses the potential and uniqueness for studying PD gastrointestinal dysfunction.
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