ArticleActa neuropathologica communications2018
A53T-α-synuclein overexpression in murine locus coeruleus induces Parkinson's disease-like pathology in neurons and glia.
Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06710574 (Multimodal Image Technologies Investigate the Role and Mechanism of Probiotics in Improving Rapid Eye Movement Behavior Disorder with Parkinson's Disease), which is not on this map. Cited by 33 papers.
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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.
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Multimodal Image Technologies Investigate the Role and Mechanism of Probiotics in Improving Rapid Eye Movement Behavior Disorder with Parkinson's Disease
Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Selective vulnerability of monoaminergic neurons and network spread of alpha-synuclein jointly explain pathology progression in Parkinson's disease models.Neurobiology of disease · 2026Article
- Locus coeruleus α-synuclein overexpression induces prodromal Parkinsonian features in mice.NPJ Parkinson's disease · 2026Article
- Mapping cellular vulnerability in Parkinson's disease using retro-AAVs and preformed α-synuclein fibrils.Translational neurodegeneration · 2026Article
- Progressive noradrenergic degeneration and motor cortical dysfunction in Parkinson's disease.Acta pharmacologica Sinica · 2025Review
- Pharmacological targeting of dopamine D1 or D2 receptors evokes a rapid-onset parkinsonian motor phenotype in mice.The European journal of neuroscience · 2024Article
- Efficient characterization of multiple binding sites of small molecule imaging ligands on amyloid-beta, tau and alpha-synuclein.European journal of nuclear medicine and molecular imaging · 2024Article
- α-Synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons at-risk in Parkinson's disease.Molecular neurodegeneration · 2024Article
- The AAV-α-Synuclein Model of Parkinson's Disease: An Update.Journal of Parkinson's disease · 2024Review
- Review
- Brain-to-gut trafficking of alpha-synuclein by CD11cNature communications · 2023Article
- The noradrenergic subtype of Parkinson disease: from animal models to clinical practice.Nature reviews. Neurology · 2023Review
- Distinct Effects of Familial Parkinson's Disease-Associated Mutations on α-Synuclein Phase Separation and Amyloid Aggregation.Biomolecules · 2023Article
- Evaluation of ferritin and TfR level in plasma neural-derived exosomes as potential markers of Parkinson's disease.Frontiers in aging neuroscience · 2023Article
- Overexpression-Induced α-Synuclein Brain Spreading.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- α-Synuclein at the Presynaptic Axon Terminal as a Double-Edged Sword.Biomolecules · 2022Review
- Human α-synuclein overexpression in mouse serotonin neurons triggers a depressive-like phenotype. Rescue by oligonucleotide therapy.Translational psychiatry · 2022Article
- Enhanced firing of locus coeruleus neurons and SK channel dysfunction are conserved in distinct models of prodromal Parkinson's disease.Scientific reports · 2022Article
- Sleep and circadian rhythms in Parkinson's disease and preclinical models.Molecular neurodegeneration · 2022Review
- The Prion-Like Spreading of Alpha-Synuclein in Parkinson's Disease: Update on Models and Hypotheses.International journal of molecular sciences · 2021Review
- Neuroprotection of Exendin-4 by Enhanced Autophagy in a Parkinsonian Rat Model of α-Synucleinopathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Degeneration of noradrenergic locus coeruleus neurons occurs during the prodromal phase of Parkinson's disease and contributes to a variety of non-motor symptoms, e.g. depression, anxiety and REM sleep behavior disorder. This study was designed to establish the first locus coeruleus α-synucleinopathy mouse model, which should provide sufficient information about the time-course of noradrenergic neurodegeneration, replicate cardinal histopathological features of the human Parkinson's disease neuropathology and finally lead to robust histological markers, which are sufficient to assess the pathological changes in a quantitative and qualitative way. We show that targeted viral vector-mediated overexpression of human mutant A53T-α-synuclein in vivo in locus coeruleus neurons of wild-type mice resulted in progressive noradrenergic neurodegeneration over a time frame of 9 weeks. Observed neuronal cell loss was accompanied by progressive α-synuclein phosphorylation, formation of proteinase K-resistant α-synuclein-aggregates, accumulation of Ubi-1- and p62-positive inclusions in microglia and induction of progressive micro- and astrogliosis. Apart from this local pathology, abundant α-synuclein-positive axons were found in locus coeruleus output regions, indicating rapid anterograde axonal transport of A53T-α-synuclein. Taken together, we present the first model of α-synucleinopathy in the murine locus coeruleus, replicating essential morphological features of human Parkinson's disease pathology. This new model may contribute to the research on prodromal Parkinson's disease, in respect to pathophysiology and the development of disease-modifying therapy.
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