ArticleFrontiers in neuroscience2016
Anle138b Partly Ameliorates Motor Deficits Despite Failure of Neuroprotection in a Model of Advanced Multiple System Atrophy.
Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- α-Synuclein pathology as a target in neurodegenerative diseases.Nature reviews. Neurology · 2025Review
- "Prion-like" seeding and propagation of oligomeric protein assemblies in neurodegenerative disorders.Frontiers in neuroscience · 2024Review
- Inhibition of Protein Aggregation and Endoplasmic Reticulum Stress as a Targeted Therapy for α-Synucleinopathy.Pharmaceutics · 2023Review
- Alpha Synuclein: Neurodegeneration and Inflammation.International journal of molecular sciences · 2023Review
- Development of Small Molecules Targeting α-Synuclein Aggregation: A Promising Strategy to Treat Parkinson's Disease.Pharmaceutics · 2023Review
- In Silico Study of the Interactions of Anle138b Isomer, an Inhibitor of Amyloid Aggregation, with Partner Proteins.International journal of molecular sciences · 2022Article
- Disease modification in Parkinsonism: obstacles and ways forward.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Therapeutics in the Pipeline TargetingPharmacological reviews · 2022Review
- Alpha-Synuclein PET Tracer Development-An Overview about Current Efforts.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Effects of pharmacological modulators of α-synuclein and tau aggregation and internalization.Scientific reports · 2020Article
- In Search of Effective Treatments Targeting α-Synuclein Toxicity in Synucleinopathies: Pros and Cons.Frontiers in cell and developmental biology · 2020Review
- Novel approaches to counter protein aggregation pathology in Parkinson's disease.Progress in brain research · 2020Review
- The small molecule inhibitor anle145c thermodynamically traps human islet amyloid peptide in the form of non-cytotoxic oligomers.Scientific reports · 2019Article
- The molecular tweezer CLR01 reduces aggregated, pathologic, and seeding-competent α-synuclein in experimental multiple system atrophy.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Iron-mediated aggregation and toxicity in a novel neuronal cell culture model with inducible alpha-synuclein expression.Scientific reports · 2019Article
- Anle138b modulates α-synuclein oligomerization and prevents motor decline and neurodegeneration in a mouse model of multiple system atrophy.Movement disorders : official journal of the Movement Disorder Society · 2019Article
- Neuroprotection by Epigenetic Modulation in a Transgenic Model of Multiple System Atrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The neurodegenerative disorder multiple system atrophy (MSA) is characterized by autonomic failure, cerebellar ataxia and parkinsonism in any combination associated with predominantly oligodendroglial α-synuclein (α-syn) aggregates (glial cytoplasmic inclusions = GCIs). To date, there is no effective disease modifying therapy. Previous experiments have shown that the aggregation inhibitor anle138b reduces neurodegeneration, as well as behavioral deficits in both transgenic and toxin mouse models of Parkinson's disease (PD). Here we analyzed whether anle138b improves motor skills and reduces neuronal loss, as well as oligodendroglial α-syn aggregation in the PLP-α-syn transgenic mouse challenged with the mitochondrial toxin 3-nitropropionic acid (3-NP) to model full-blown MSA. Following 1 month of treatment with anle138b, MSA mice showed signs of motor improvement affecting stride length, but not pole, grip strength, and beam test performance. Loss of dopaminergic nigral neurons and Purkinje cells was not attenuated and GCI density remained unchanged. These data suggest that the pathology in transgenic PLP-α-syn mice receiving 3-NP might be too advanced to detect significant effects of anle138b treatment on neuronal loss and intracytoplasmic α-syn inclusion bodies. However, the partial motor amelioration may indicate potential efficacy of anle138b treatment that may be mediated by its actions on α-syn oligomers or may reflect improvement of neuronal dysfunction in neural at risk populations. Further studies are required to address the efficacy of anle138b in transgenic α-syn models of early-stage MSA and in the absence of additional toxin application.
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Registered trials
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