ArticleActa neuropathologica communications2021
Robust α-synuclein pathology in select brainstem neuronal populations is a potential instigator of multiple system atrophy.
Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- α-Synuclein overexpression increases the tropism of pre-formed fibrils and MSA-patient derived seeds towards oligodendroglia.Acta neuropathologica communications · 2026Article
- Multiple system atrophy: advances in pathogenesis and emerging therapeutic strategies.Journal of neurology · 2025Review
- Autonomic dysfunction in multiple system atrophy: from pathophysiology to clinical manifestations.Annals of medicine · 2025Review
- Contribution of α-synuclein cytopathologies to distinct seeding of misfolded α-synuclein.Brain pathology (Zurich, Switzerland) · 2025Article
- Brain structural features with functional priori to classify Parkinson's disease and multiple system atrophy using diagnostic MRI.Scientific reports · 2025Article
- Lewy-MSA hybrid fold drives distinct neuronal α-synuclein pathology.Communications biology · 2025Article
- Fibrinogen degradation products exacerbate alpha-synuclein aggregation by inhibiting autophagy via downregulation of Beclin1 in multiple system atrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- N-terminus α-synuclein detection reveals new and more diverse aggregate morphologies in multiple system atrophy and Parkinson's disease.Translational neurodegeneration · 2024Article
- Optimization of Parkinson's disease therapy with plant extracts and nutrition's evolving roles.IBRO neuroscience reports · 2024Review
- Distinct ultrastructural phenotypes of glial and neuronal alpha-synuclein inclusions in multiple system atrophy.Brain : a journal of neurology · 2024Article
- A novel mouse model for investigating α-synuclein aggregates in oligodendrocytes: implications for the glial cytoplasmic inclusions in multiple system atrophy.Molecular brain · 2024Article
- The Vocal Flutter of Multiple System Atrophy: A Parkinsonian-Type Phenomenon?Movement disorders clinical practice · 2024Review
- Cellular processing of α-synuclein fibrils results in distinct physiological C-terminal truncations with a major cleavage site at residue Glu 114.The Journal of biological chemistry · 2023Article
- Multiple system atrophy: at the crossroads of cellular, molecular and genetic mechanisms.Nature reviews. Neuroscience · 2023Review
- Oligodendrocytes Prune Axons Containing α-Synuclein Aggregates In Vivo: Lewy Neurites as Precursors of Glial Cytoplasmic Inclusions in Multiple System Atrophy?Biomolecules · 2023Article
- Multiple system atrophy.Nature reviews. Disease primers · 2022Review
- Unique seeding profiles and prion-like propagation of synucleinopathies are highly dependent on the host in human α-synuclein transgenic mice.Acta neuropathologica · 2022Article
- Long-standing multiple system atrophy-Parkinsonism with limbic and FTLD-type α-synuclein pathology.Neuropathology and applied neurobiology · 2022Article
- Is Multiple System Atrophy a Prion-like Disorder?International journal of molecular sciences · 2021Review
- Disease-, region- and cell type specific diversity of α-synuclein carboxy terminal truncations in synucleinopathies.Acta neuropathologica communications · 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Multiple system atrophy (MSA) is an insidious middle age-onset neurodegenerative disease that clinically presents with variable degrees of parkinsonism and cerebellar ataxia. The pathological hallmark of MSA is the progressive accumulation of glial cytoplasmic inclusions (GCIs) in oligodendrocytes that are comprised of α-synuclein (αSyn) aberrantly polymerized into fibrils. Experimentally, MSA brain samples display a high level of seeding activity to induce further αSyn aggregation by a prion-like conformational mechanism. Paradoxically, αSyn is predominantly a neuronal brain protein, with only marginal levels expressed in normal or diseased oligodendrocytes, and αSyn inclusions in other neurodegenerative diseases, including Parkinson's disease and Dementia with Lewy bodies, are primarily found in neurons. Although GCIs are the hallmark of MSA, using a series of new monoclonal antibodies targeting the carboxy-terminal region of αSyn, we demonstrate that neuronal αSyn pathology in MSA patient brains is remarkably abundant in the pontine nuclei and medullary inferior olivary nucleus. This neuronal αSyn pathology has distinct histological properties compared to GCIs, which allows it to remain concealed to many routine detection methods associated with altered biochemical properties of the carboxy-terminal domain of αSyn. We propose that these previously underappreciated sources of aberrant αSyn could serve as a pool of αSyn prion seeds that can initiate and continue to drive the pathogenesis of MSA.
Indexed as
Identifiers
What OpenQuestion holds
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.