Evidence map›Paper›PMID 35327402›Full record

ReviewBiomedicines2022

Heterogeneity of Multiple System Atrophy: An Update.

Kurt A Jellinger

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
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  4. Exidavnemab binds to aggregated α-synuclein in human brains affected by α-synucleinopathies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Mild cognitive impairment in multiple system atrophy: a brain network disorder.Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Kurt A JellingerInstitute of Clinical Neurobiology, Alberichgasse 5/13, A-1150 Vienna, Austria.ORCID 0000-0002-9641-7649

Funding

Society for the Promotion of Research in Experimental Neurology, Vienna, Austria 001
6 · The paper itself

Abstract

Multiple system atrophy (MSA) is a fatal, rapidly progressing neurodegenerative disease of uncertain etiology, clinically characterized by various combinations of Levodopa unresponsive parkinsonism, cerebellar, autonomic and motor dysfunctions. The morphological hallmark of this α-synucleinopathy is the deposition of aberrant α-synuclein in both glia, mainly oligodendroglia (glial cytoplasmic inclusions /GCIs/) and neurons, associated with glioneuronal degeneration of the striatonigral, olivopontocerebellar and many other neuronal systems. Typical phenotypes are MSA with predominant parkinsonism (MSA-P) and a cerebellar variant (MSA-C) with olivocerebellar atrophy. However, MSA can present with a wider range of clinical and pathological features than previously thought. In addition to rare combined or "mixed" MSA, there is a broad spectrum of atypical MSA variants, such as those with a different age at onset and disease duration, "minimal change" or prodromal forms, MSA variants with Lewy body disease or severe hippocampal pathology, rare forms with an unusual tau pathology or spinal myoclonus, an increasing number of MSA cases with cognitive impairment/dementia, rare familial forms, and questionable conjugal MSA. These variants that do not fit into the current classification of MSA are a major challenge for the diagnosis of this unique proteinopathy. Although the clinical diagnostic accuracy and differential diagnosis of MSA have improved by using combined biomarkers, its distinction from clinically similar extrapyramidal disorders with other pathologies and etiologies may be difficult. These aspects should be taken into consideration when revising the current diagnostic criteria. This appears important given that disease-modifying treatment strategies for this hitherto incurable disorder are under investigation.

Indexed as

atypical formsclinico-pathological variantsconjugal MSA“minimal change” MSAMSA with hippocampal pathologyMSA with lewy bodiesmultiple system atrophy

Identifiers

PMID35327402
PMCPMC8945102
OpenAlexW4214812960

What OpenQuestion holds

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Registered trials

None linked

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.