Evidence map›Paper›PMID 33639338›Full record

ArticleNeurobiology of aging2021

Age-related increase of alpha-synuclein oligomers is associated with motor disturbances in L61 transgenic mice.

Sahar Roshanbin, Agata Aniszewska, Astrid Gumucio, Eliezer Masliah, Anna Erlandsson, Joakim Bergström, Martin Ingelsson, Sara Ekmark-Lewén

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. 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

8 authors at 2 institutions in 2 countries.

Sahar RoshanbinDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Agata AniszewskaDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Astrid GumucioDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Eliezer MasliahDivision of Neurosciences, NIA-NIH, Bethesda, USA.
Anna ErlandssonDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Joakim BergströmDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Martin IngelssonDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Sara Ekmark-LewénDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden. Electronic address: sara.ekmark-lewen@pubcare.uu.se.
Uppsala University · SENational Institutes of Health · US

Funding

Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA AG000936
6 · The paper itself

Abstract

The pathogenesis of Parkinson's disease involves fibrillization and deposition of alpha-synuclein (α-syn) into Lewy bodies. Accumulating evidence suggests that α-syn oligomers are particularly neurotoxic. Transgenic (tg) mice overexpressing wild-type human α-syn under the Thy-1 promoter (L61) reproduce many Parkinson's disease features, but the pathogenetic relevance of α-syn oligomers in this mouse model has not been studied in detail. Here, we report an age progressive increase of α-syn oligomers in the brain of L61 tg mice. Interestingly, more profound motor symptoms were observed in animals with higher levels of membrane-bound oligomers. As this tg model is X-linked, we also performed subset analyses, indicating that both sexes display a similar age-related increase in α-syn oligomers. However, compared with females, males featured increased brain levels of oligomers from an earlier age, in addition to a more severe behavioral phenotype with hyperactivity and thigmotaxis in the open field test. Taken together, our data indicate that α-syn oligomers are central to the development of brain pathology and behavioral deficits in the L61 tg α-syn mouse model.

Indexed as

Agingalpha-SynucleinAnimalsDisease Models, AnimalFemaleGene ExpressionLewy BodiesMaleMice, TransgenicParkinson DiseasePromoter Regions, GeneticThy-1 Antigensalpha-SynucleinThy-1 AntigensAge progressionAggregationAlpha-synucleinDementia with Lewy bodiesOligomersParkinson's diseaseSex differencesThy-1Transgenic mice

Identifiers

PMID33639338
PMCPMC9648497
OpenAlexW3125356116

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.