ReviewBrain and behavior2022
Modeling Parkinson's disease-related symptoms in alpha-synuclein overexpressing mice.
Review in Brain and behavior, 2022. 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, 39 citations in OpenAlex.
- Preclinical evaluation of nitrated α-synuclein-specific CAR-Treg therapy in Parkinson's disease.Cell reports. Medicine · 2026Article
- Neuronal overexpression of Kcnn1 in A53T α-synuclein mice suppresses phospho-serine 129 α-synuclein formation and doubles survival time.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The epitranscriptomic m6A RNA modification modulates the synapse in ageing and in a mouse model of synucleinopathy.NPJ Parkinson's disease · 2026Article
- Novel Insights Into the Association Between Parkinson's Disease and Constipation: Role of SHMT2 as a Promising Biomarker.CNS neuroscience & therapeutics · 2026Article
- Comparative Analysis of T-Cell Signatures and Astroglial Reactivity in Parkinson's Pathology Across Animal Models with Distinct Regenerative Capacities.International journal of molecular sciences · 2026Article
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- Alpha-Synuclein Neurobiology in Parkinson's Disease: A Comprehensive Review of Its Role, Mechanisms, and Therapeutic Perspectives.Brain sciences · 2025Review
- Inherited Genetic Variation in Parkinson's Disease: Convergence on Impaired Autophagosome-Lysosome Fusion Through the Altered Expression of mRNA Isoforms.Molecular neurobiology · 2025Article
- Integrating artificial intelligence and optogenetics for Parkinson's disease diagnosis and therapeutics in male mice.Nature communications · 2025Article
- Elevated plasma levels of alpha-synuclein are dispensable for Parkinson's disease pathology.NPJ Parkinson's disease · 2025Article
- Mechanosensitive ion channels and inflammation: key links in cellular signal transduction.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Bradykinesia and postural instability in a model of prodromal synucleinopathy with α-synuclein aggregation initiated in the gigantocellular nuclei.Acta neuropathologica communications · 2025Article
- α-Synuclein pathology as a target in neurodegenerative diseases.Nature reviews. Neurology · 2025Review
- Drug discovery and development for Parkinson's disease: are preclinical models good enough?Frontiers in aging neuroscience · 2025Review
- Experimental Models to Study Immune Dysfunction in the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2024Review
- α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce CaTranslational neurodegeneration · 2024Article
- A Novel NOX Inhibitor Alleviates Parkinson's Disease Pathology in PFF-Injected Mice.International journal of molecular sciences · 2023Article
- Intensive exercise ameliorates motor and cognitive symptoms in experimental Parkinson's disease restoring striatal synaptic plasticity.Science advances · 2023Article
- Multilingual evaluation of interpretable biomarkers to represent language and speech patterns in Parkinson's disease.Frontiers in neurology · 2023Article
- Single point mutations at the S129 residue of α-synuclein and their effect on structure, aggregation, and neurotoxicity.Frontiers in chemistry · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracellular deposition of alpha-synuclein (α-syn) as Lewy bodies and Lewy neurites is a central event in the pathogenesis of Parkinson's disease (PD) and other α-synucleinopathies. Transgenic mouse models overexpressing human α-syn, are useful research tools in preclinical studies of pathogenetic mechanisms. Such mice develop α-syn inclusions as well as neurodegeneration with a topographical distribution that varies depending on the choice of promoter and which form of α-syn that is overexpressed. Moreover, they display motor symptoms and cognitive disturbances that to some extent resemble the human conditions. PURPOSE: One of the main motives for assessing behavior in these mouse models is to evaluate the potential of new treatment strategies, including their impact on motor and cognitive symptoms. However, due to a high within-group variability with respect to such features, the behavioral studies need to be applied with caution. In this review, we discuss how to make appropriate choices in the experimental design and which tests that are most suitable for the evaluation of PD-related symptoms in such studies.
methodsWe have evaluated published results on two selected transgenic mouse models overexpressing wild type (L61) and mutated (A30P) α-syn in the context of their validity and utility for different types of behavioral studies.
conclusionsBy applying appropriate behavioral tests, α-syn transgenic mouse models provide an appropriate experimental platform for studies of symptoms related to PD and other α-synucleinopathies.
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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.