ReviewAutonomic neuroscience : basic & clinical2018
The neuropathology of multiple system atrophy and its therapeutic implications.
Review in Autonomic neuroscience : basic & clinical, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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.
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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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Differentially Expressed miRNAs in Age-Related Neurodegenerative Diseases: A Meta-Analysis.Genes · 2022Pooled it
- Cutaneous alpha-synuclein deposition informs autonomic function in individuals with early-stage multiple system atrophy.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026Article
- Feasibility of short imaging protocols for [European journal of nuclear medicine and molecular imaging · 2026Article
- Structure-function relationship of alpha-synuclein fibrillar polymorphs derived from distinct synucleinopathies.Molecular systems biology · 2026Article
- Review
- Review
- Proximity proteomics reveals unique and shared pathological features between multiple system atrophy and Parkinson's disease.Acta neuropathologica communications · 2025Article
- Gradients of Nigrostriatal Iron Deposition in Healthy Aging and Synucleinopathies.CNS neuroscience & therapeutics · 2025Article
- Toward a biological definition of neuronal and glial synucleinopathies.Nature medicine · 2025Review
- Distinct ultrastructural phenotypes of glial and neuronal alpha-synuclein inclusions in multiple system atrophy.Brain : a journal of neurology · 2024Article
- Comparing alpha-synuclein-interactomes between multiple systems atrophy and Parkinson's disease reveals unique and shared pathological features.bioRxiv : the preprint server for biology · 2024Article
- Multiple system atrophy: an update and emerging directions of biomarkers and clinical trials.Journal of neurology · 2024Review
- Distinct forebrain regions define a dichotomous astrocytic profile in multiple system atrophy.Acta neuropathologica communications · 2024Article
- Ultrastructures of α-Synuclein Filaments in Synucleinopathy Brains and Experimental Models.Journal of movement disorders · 2024Article
- Gene Set Enrichment Analysis and Genetic Experiment Reveal Changes in Cell Signaling Pathways Induced by α-Synuclein Overexpression.Biomedicines · 2023Article
- Clinical outcomes and cognitive impairments between progressive supranuclear palsy and multiple system atrophy.Brain and behavior · 2022Article
- The potential convergence of NLRP3 inflammasome, potassium, and dopamine mechanisms in Parkinson's disease.NPJ Parkinson's disease · 2022Review
- Depression in multiple system atrophy: Views on pathological, clinical and imaging aspects.Frontiers in psychiatry · 2022Review
- Discrimination of MSA-P and MSA-C by RT-QuIC analysis of olfactory mucosa: the first assessment of assay reproducibility between two specialized laboratories.Molecular neurodegeneration · 2021Article
- Alpha-Synuclein PET Tracer Development-An Overview about Current Efforts.Pharmaceuticals (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple system atrophy (MSA) is a fatal neurodegenerative disorder characterized by the abnormal accumulation of toxic forms of the synaptic protein alpha-synuclein (α-syn) within oligodendrocytes and neurons. The presence of α-syn within oligodendrocytes in the form of glial cytoplasmic inclusions is the diagnostic hallmark of MSA. However, it has been postulated that α-syn is produced in neurons and propagates to oligodendrocytes, where unknown mechanisms lead to its accumulation. The presence of α-syn within neurons in MSA has not been so extensively studied, but it may shed light into neuropathological mechanisms leading to oligodendroglial accumulation. Here we summarize the principal neuropathological events of MSA, and discuss how a deeper knowledge of these mechanisms may help develop effective therapies targeting α-syn accumulation and spreading.
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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.