ArticleHuman molecular genetics2015
Early Parkinson's disease symptoms in α-synuclein transgenic monkeys.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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.
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Who cites it
55 citing papers in PubMed, 98 citations in OpenAlex.
- α-Synuclein aggregation and brain atrophy in SNCA-A53T transgenic monkeys are correlated with parkinsonism.Brain : a journal of neurology · 2026Article
- Modeling Tau-Mediated Pathology in Monkey Brain Slices.Biology · 2026Article
- Genetically Modified Primate Models for Brain Disorder Research.Neuroscience bulletin · 2026Review
- Article
- Position paper: leveraging non-human primate (NHP) specificities to accelerate Parkinson's disease and ageing research.NPJ Parkinson's disease · 2025Review
- Differential pathological dynamics triggered by distinct Parkinson patient-derived α-synuclein extracts in nonhuman primates.Science advances · 2025Article
- An update on mammalian and non-mammalian animal models for biomarker development in neurodegenerative disorders.Cellular and molecular life sciences : CMLS · 2025Review
- Liver-specific transgenic expression of human NTCP in rhesus macaques confers HBV susceptibility on primary hepatocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Drug discovery and development for Parkinson's disease: are preclinical models good enough?Frontiers in aging neuroscience · 2025Review
- Genetically modified non-human primate models for research on neurodegenerative diseases.Zoological research · 2024Review
- Opioid abuse and SIV infection in non-human primates.Journal of neurovirology · 2023Review
- A controlled ovarian stimulation procedure suitable for cynomolgus macaques.Experimental animals · 2022Article
- New pathogenic insights from large animal models of neurodegenerative diseases.Protein & cell · 2022Review
- Review
- Modeling genetic diseases in nonhuman primates through embryonic and germline modification: Considerations and challenges.Science translational medicine · 2022Review
- Serum- and Feeder-Free Culture of Juvenile Monkey Female Germline Stem Cells and Testosterone Regulation of their Self-Renewal.Stem cell reviews and reports · 2022Article
- Evaluating depression- and anxiety-like behaviors in non-human primates.Frontiers in behavioral neuroscience · 2022Review
- Gene editing monkeys: Retrospect and outlook.Frontiers in cell and developmental biology · 2022Review
- Genetically modified large animal models for investigating neurodegenerative diseases.Cell & bioscience · 2021Review
- Gut microbiota and metabolites of α-synuclein transgenic monkey models with early stage of Parkinson's disease.NPJ biofilms and microbiomes · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Parkinson's disease (PD) is an age-dependent neurodegenerative disease that can be caused by genetic mutations in α-synuclein (α-syn) or duplication of wild-type α-syn; PD is characterized by the deposition of α-syn aggregates, indicating a gain of toxicity from accumulation of α-syn. Although the major neuropathologic feature of PD is the degeneration of dopaminergic (DA) neurons in the substantia nigra, non-motor symptoms including anxiety, cognitive defect and sleep disorder precede the onset of motor impairment, and many clinical symptoms of PD are not caused by degeneration of DA neurons. Non-human primate models of PD are important for revealing the early pathology in PD and identifying effective treatments. We established transgenic PD rhesus monkeys that express mutant α-syn (A53T). Six transgenic A53T monkeys were produced via lentiviral vector expressing A53T in fertilized monkey eggs and subsequent embryo transfer to surrogates. Transgenic A53T is expressed in the monkey brain and causes age-dependent non-motor symptoms, including cognitive defects and anxiety phenotype, without detectable sleeping disorders. The transgenic α-syn monkeys demonstrate the specific early symptoms caused by mutant α-syn and provide insight into treatment of early PD.
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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.