Evidence map›Paper›PMID 31508228›Full record

ReviewTranslational neurodegeneration2019

Beyond the synucleinopathies: alpha synuclein as a driving force in neurodegenerative comorbidities.

Naomi P Visanji, Anthony E Lang, Gabor G Kovacs

Open access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Comorbid pathologies and their impact on progressive supranuclear palsy: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  5. Comorbid pathologies and their impact on multiple system atrophy: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. The role ofFrontiers in neuroscience · 2025
    Review
  12. Article
  13. Review
  14. Associations between misfolded alpha-synuclein aggregates and Alzheimer's disease pathology in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

3 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Naomi P Visanji1Edmond J. Safra program in Parkinson's disease and the Morton and Gloria Shulman Movement disorders clinic, Toronto Western Hospital, Toronto, Ontario Canada.ORCID 0000-0001-5968-7845
Anthony E Lang1Edmond J. Safra program in Parkinson's disease and the Morton and Gloria Shulman Movement disorders clinic, Toronto Western Hospital, Toronto, Ontario Canada.
Gabor G Kovacs1Edmond J. Safra program in Parkinson's disease and the Morton and Gloria Shulman Movement disorders clinic, Toronto Western Hospital, Toronto, Ontario Canada.
Toronto Western Hospital · CAUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The fundamental role that alpha-synuclein (aSyn) plays in the pathogenesis of neurodegenerative synucleinopathies, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, is a well-accepted fact. A wealth of experimental evidence has linked this relatively small but ubiquitously expressed protein to a plethora of cytopathologic mechanisms and suggests that aSyn may be capable of seeding the progressive spread of synucleinopathy throughout the brain. Beyond the synucleinopathies, the abnormal deposition of aSyn is frequently seen in a variety of other neurodegenerative proteinopathies including Alzheimer's disease. In spite of the fact that the frequency of concomitant aSyn pathology in these disorders is such that it can be considered the rule rather than the exception, the potential role that aSyn may have in these disorders has received relatively little attention. In this article we postulate that aSyn may in fact be a key protein in driving the pathogenic processes in neurodegenerative comorbidities. In addition to reviewing the frequency of concomitant deposition of aSyn in the neurodegenerative proteinopathies, we also consider our current understanding of the interaction of aSyn with other neurodegenerative disease-associated proteins, including tau, TDP-43, amyloid-β and prion protein, in the context of neuropathologic studies describing the anatomical sites of potential concomitant pathology. We conclude that a growing body of evidence, encompassing neuropathology studies in human brain, animal models of concomitant proteinopathies and studies employing sophisticated methods of probing protein-protein interaction, cumulatively suggest that aSyn is well positioned to exert a strong influence on the pathogenesis of the neurodegenerative comorbidities. We hope to stimulate research in this emerging field and consider that future studies exploring the contribution of aSyn to the pathogenic processes in neurodegenerative comorbidities may provide critical information pertaining to diagnosis and the development of vital disease modifying treatments for these devastating diseases.

Indexed as

Alpha-synucleinAlzheimer’s diseaseAmyloid-βComorbidityDementia with Lewy bodiesMultiple system atrophyNeurodegenerationParkinson’s diseasePrion proteinProgressive supranuclear palsyProteinopathyTauTDP-43

Identifiers

PMID31508228
PMCPMC6727368
OpenAlexW2971670235

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.