ArticleHuman molecular genetics2010
Extensive enteric nervous system abnormalities in mice transgenic for artificial chromosomes containing Parkinson disease-associated alpha-synuclein gene mutations precede central nervous system changes.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
149 citing papers in PubMed, 285 citations in OpenAlex.
- Trial
- Colonic biopsies to assess the neuropathology of Parkinson's disease and its relationship with symptoms.PloS one · 2010Trial
- α-Synuclein aggregation and brain atrophy in SNCA-A53T transgenic monkeys are correlated with parkinsonism.Brain : a journal of neurology · 2026Article
- Knockout of α-Synuclein Is Associated with Depression-like Behaviors by Altered Excitability of Medial Prefrontal Cortex Neurons in Mice.International journal of molecular sciences · 2026Article
- Strategies for Optimizing Genetic Mouse Models to Enhance the Understanding of Parkinson's Disease.Biomedicines · 2026Review
- Early intestinal barrier changes in A53T transgenic Parkinson's disease mice.Cell and tissue research · 2026Article
- Fluorescence Detection of Alpha-Synuclein Aggregates in the Gut Using a Peptide Probe.ACS chemical neuroscience · 2026Article
- The Microbiome-Neurodegeneration Interface: Mechanisms, Evidence, and Future Directions.Cells · 2026Review
- Article
- Templating of monomeric alpha-synuclein results in inflammation and SNpc dopamine neuron death in a genetic mouse model of induced synucleinopathy.Scientific reports · 2025Article
- The interrelationship between intestinal immune cells and enteric α-synuclein in the progression of Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Assessment of gastrointestinal function and enteric nervous system changes over time in the A53T mouse model of Parkinson's disease.Acta neuropathologica communications · 2025Article
- Limitations and Applications of Rodent Models in Tauopathy and Synucleinopathy Research.Journal of neurochemistry · 2025Review
- Chronic DSS-Induced Colitis Exacerbates Parkinson's Disease Phenotype and Its Pathological Features Following Intragastric Rotenone Exposure.ACS pharmacology & translational science · 2025Article
- Polystyrene Nanoplastics Hitch-Hike the Gut-Brain Axis to Exacerbate Parkinson's Pathology.ACS nano · 2025Article
- Longitudinal characterization reveals behavioral impairments in aged APP knock in mouse models.Scientific reports · 2025Article
- Drug discovery and development for Parkinson's disease: are preclinical models good enough?Frontiers in aging neuroscience · 2025Review
- Optimization of protocols for immunohistochemical assessment of enteric nervous system in formalin fixed human tissue.bioRxiv : the preprint server for biology · 2024Article
- Chronic urinary tract infections cause persistent microglial changes in a humanized ɑ-synuclein mouse model.Journal of Parkinson's disease · 2024Article
- Review
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 1 country.
Funding
Abstract
Parkinson disease (PD) is a neurodegenerative disease with motor as well as non-motor signs in the gastrointestinal tract that include dysphagia, gastroparesis, prolonged gastrointestinal transit time, constipation and difficulty with defecation. The gastrointestinal dysfunction commonly precedes the motor symptoms by decades. Most PD is sporadic and of unknown etiology, but a fraction is familial. Among familial forms of PD, a small fraction is caused by missense (A53T, A30P and E46K) and copy number mutations in SNCA which encodes alpha-synuclein, a primary protein constituent of Lewy bodies, the pathognomonic protein aggregates found in neurons in PD. We set out to develop transgenic mice expressing mutant alpha-synuclein (either A53T or A30P) from insertions of an entire human SNCA gene as models for the familial disease. Both the A53T and A30P lines show robust abnormalities in enteric nervous system (ENS) function and synuclein-immunoreactive aggregates in ENS ganglia by 3 months of age. The A53T line also has abnormal motor behavior but neither demonstrates cardiac autonomic abnormalities, olfactory dysfunction, dopaminergic neurotransmitter deficits, Lewy body inclusions or neurodegeneration. These animals recapitulate the early gastrointestinal abnormalities seen in human PD. The animals also serve as an in vivo system in which to investigate therapies for reversing the neurological dysfunction that target alpha-synuclein toxicity at its earliest stages.
Indexed as
Identifiers
What OpenQuestion holds
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.