Evidence map›Paper›PMID 27550225›Full record

ArticleActa neuropathologica communications2016

Telomere shortening leads to an acceleration of synucleinopathy and impaired microglia response in a genetic mouse model.

Annika Scheffold, Inge R Holtman, Sandra Dieni, Nieske Brouwer, Sarah-Fee Katz, Billy Michael Chelliah Jebaraj, Philipp J Kahle, Bastian Hengerer, André Lechel, Stephan Stilgenbauer and 4 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. lncRNAbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Ageing in the brain: mechanisms and rejuvenating strategies.Cellular and molecular life sciences : CMLS · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Neurons and Glia Interplay in α-Synucleinopathies.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Microglia in neurodegenerative diseases.Neural regeneration research · 2021
    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

14 authors at 7 institutions in 2 countries.

Annika ScheffoldDepartment of Internal Medicine III, University of Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Inge R HoltmanDepartment of Neuroscience, Section Medical Physiology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands.
Sandra DieniDepartment for Psychiatry and Psychotherapy, Molecular Psychiatry, Freiburg University Hospital, Hauptstrasse 5, 79104, Freiburg, Germany.
Nieske BrouwerDepartment of Neuroscience, Section Medical Physiology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands.
Sarah-Fee KatzDepartment of Internal Medicine I, University of Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Billy Michael Chelliah JebarajDepartment of Internal Medicine III, University of Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Philipp J KahleCenter of Neurology and Hertie-Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Bastian HengererBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
André LechelDepartment of Internal Medicine I, University of Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Stephan StilgenbauerDepartment of Internal Medicine III, University of Ulm, Albert-Einstein-Allee 23, 89081, Ulm, Germany.
Erik W G M BoddekeDepartment of Neuroscience, Section Medical Physiology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands.
Bart J L EggenDepartment of Neuroscience, Section Medical Physiology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands.
Karl-Lenhard RudolphLeibniz Institute for Age Research, Beutenbergstr. 11, 07745, Jena, Germany.
Knut BiberDepartment of Neuroscience, Section Medical Physiology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands. knut.biber@uniklinik-freiburg.de.
Universität Ulm · DEUniversity Medical Center Freiburg · DEUniversity Medical Center Groningen · NLUniversity of Groningen · NLBoehringer Ingelheim (Germany) · DEHertie Institute for Clinical Brain Research · DELeibniz Association · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is one of the most common neurodegenerative disorders of the elderly and ageing hence described to be a major risk factor. Telomere shortening as a result of the inability to fully replicate the ends of linear chromosomes is one of the hallmarks of ageing. The role of telomere dysfunction in neurological diseases and the ageing brain is not clarified and there is an ongoing discussion whether telomere shortening is linked to Parkinson's disease. Here we studied a mouse model of Parkinson's disease (Thy-1 [A30P] α-synuclein transgenic mouse model) in the background of telomere shortening (Terc knockout mouse model). α-synuclein transgenic mice with short telomeres (αSYN(tg/tg) G3Terc(-/-)) developed an accelerated disease with significantly decreased survival. This accelerated phenotype of mice with short telomeres was characterized by a declined motor performance and an increased formation of α-synuclein aggregates. Immunohistochemical analysis and mRNA expression studies revealed that the disease end-stage brain stem microglia showed an impaired response in αSYN(tg/tg) G3Terc(-/-) microglia animals. These results provide the first experimental data that telomere shortening accelerates α-synuclein pathology that is linked to limited microglia function in the brainstem.

Indexed as

alpha-SynucleinAnimalsBrain StemDisease ProgressionHumansMice, Inbred C57BLMice, TransgenicMicrogliaMotor ActivityParkinsonian DisordersPhenotypePostural BalanceProtein Aggregation, PathologicalRNA, MessengerTelomere ShorteningTime Factorsalpha-SynucleinRNA, MessengerSNCA protein, humanMicrogliaParkinson’s diseaseTelomeresα-synuclein

Identifiers

PMID27550225
PMCPMC4994259
OpenAlexW2517605453

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.