Evidence map›Paper›PMID 29376857›Full record

ReviewJournal of Alzheimer's disease : JAD2018

The Relevance of Iron in the Pathogenesis of Multiple System Atrophy: A Viewpoint.

Christine Kaindlstorfer, Kurt A Jellinger, Sabine Eschlböck, Nadia Stefanova, Günter Weiss, Gregor K Wenning

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.2field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Tau accumulation is associated with dopamine deficiency in vivo in four-repeat tauopathies.European journal of nuclear medicine and molecular imaging · 2024
    Article
  11. The 'α-synucleinopathy syndicate': multiple system atrophy and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

6 authors at 1 institution in 1 country.

Christine KaindlstorferDepartment of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Kurt A JellingerInstitute of Clinical Neurobiology, Vienna, Austria.
Sabine EschlböckDepartment of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Nadia StefanovaDepartment of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Günter WeissDepartment of Internal Medicine, Medical University of Innsbruck, Innsbruck, Austria.
Gregor K WenningDepartment of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

Austrian Science Fund FWF I 2102
6 · The paper itself

Abstract

Iron is essential for cellular development and maintenance of multiple physiological processes in the central nervous system. The disturbance of its homeostasis leads to abnormal iron deposition in the brain and causes neurotoxicity via generation of free radicals and oxidative stress. Iron toxicity has been established in the pathogenesis of Parkinson's disease; however, its contribution to multiple system atrophy (MSA) remains elusive. MSA is characterized by cytoplasmic inclusions of misfolded α-synuclein (α-SYN) in oligodendrocytes referred to as glial cytoplasmic inclusions (GCIs). Remarkably, the oligodendrocytes possess high amounts of iron, which together with GCI pathology make a contribution toward MSA pathogenesis likely. Consistent with this observation, the GCI density is associated with neurodegeneration in central autonomic networks as well as olivopontocerebellar and striatonigral pathways. Iron converts native α-SYN into a β-sheet conformation and promotes its aggregation either directly or via increasing levels of oxidative stress. Interestingly, α-SYN possesses ferrireductase activity and α-SYN expression underlies iron mediated translational control via RNA stem loop structures. Despite a correlation between progressive putaminal atrophy and iron accumulation as well as clinical decline, it remains unclear whether pathologic iron accumulation in MSA is a secondary event in the cascade of neuronal degeneration rather than a primary cause. This review summarizes the current knowledge of iron in MSA and gives evidence for perturbed iron homeostasis as a potential pathogenic factor in MSA-associated neurodegeneration.

Indexed as

alpha-SynucleinBrainHumansInclusion BodiesIronMagnetic Resonance ImagingMultiple System AtrophyOligodendrogliaParkinsonian Disordersalpha-SynucleinIronIronmultiple system atrophyneurodegenerationParkinson’s diseaseα-SYN

Identifiers

PMID29376857
PMCPMC5798525
OpenAlexW2785002530

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.