Evidence map›Paper›PMID 11724918›Full record

ReviewMolecular pathology : MP2001

Multiple system atrophy: cellular and molecular pathology.

D J Burn, E Jaros

Abstract readReview
In one paragraph

Review in Molecular pathology : MP, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. BDNF and Cerebellar Ataxia.Current drug research reviews · 2024
    Review
  8. Clinicopathological correlates of pyramidal signs in multiple system atrophy.Annals of clinical and translational neurology · 2022
    Article
  9. Article
  10. Circulatory 25(OH)D and 1,25(OH)eNeurologicalSci · 2021
    Article
  11. Neuropathology of multiple system atrophy: Kurt Jellinger`s legacy.Journal of neural transmission (Vienna, Austria : 1996) · 2021
    Review
  12. Article
  13. Ubisol-QAntioxidants (Basel, Switzerland) · 2021
    Review
  14. Signs of early cellular dysfunction in multiple system atrophy.Neuropathology and applied neurobiology · 2021
    Article
  15. Coenzyme QInternational journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  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

2 authors at 1 institution in 1 country.

D J BurnRegional Neurosciences Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, UK. d.j.burn@ncl.ac.uk
E Jaros
North Tyneside General Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple system atrophy is an adult onset neurodegenerative disease, featuring parkinsonism, ataxia, and autonomic failure, in any combination. The condition is relentlessly progressive and responds poorly to treatment. Death occurs on average six to seven years after the onset of symptoms. No familial cases of multiple system atrophy have been reported, and no environmental factors have been robustly implicated as aetiological factors. However, analytical epidemiological studies are hampered because the condition is relatively rare. The discovery of the glial cytoplasmic inclusion (GCI) in 1989 helped to define multiple system atrophy as a clinicopathological entity, and drew attention to the prominent, if not primary, role played by the oligodendrocyte in the pathogenesis of the condition. Subsequently, GCIs were shown to be positive for alpha-synuclein, with immunostaining for this protein indicating that white matter pathology was more widespread than had previously been recognised. The presence of alpha-synuclein in GCIs provides a link with Parkinson's disease, dementia with Lewy bodies, and neurodegeneration with brain iron accumulation, type 1 (or Hallervorden-Spatz syndrome), in which alpha-synuclein is also found within Lewy bodies. This has led to the term "synucleinopathy" to embrace this group of conditions. The GCIs of multiple system atrophy contain a range of other cytoskeletal proteins. It is unknown how fibrillogenesis occurs, and whether there is primary oligodendrocytic dysfunction, which then disrupts the neurone/axon as a consequence of the glial pathology, or whether the oligodendrocytic changes merely represent an epiphenomenon. Further research into this devastating condition is urgently needed to improve our understanding of the pathogenesis, and also to produce new treatment approaches.

Indexed as

Agedalpha-SynucleinAutonomic Nervous SystemAxonsBrainBrain-Derived Neurotrophic FactorCell DeathExtracellular MatrixFemaleHumansInclusion BodiesMaleMiddle AgedMultiple System AtrophyNerve Tissue ProteinsNeuronsalpha-SynucleinBrain-Derived Neurotrophic FactorNerve Tissue ProteinsSNCA protein, humanSynucleins

Identifiers

PMID11724918
PMCPMC1187133
OpenAlexW2157262140

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.