Evidence map›Paper›PMID 26771599›Full record

ReviewInternational journal of molecular sciences2016

Insights into Mechanisms of Chronic Neurodegeneration.

Abigail B Diack, James D Alibhai, Rona Barron, Barry Bradford, Pedro Piccardo, Jean C Manson

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Prion-Like Mechanisms in Parkinson's Disease.Frontiers in neuroscience · 2019
    Review
  8. Review
  9. Article
  10. Article
  11. Prion-like mechanisms in Alzheimer disease.Handbook of clinical neurology · 2018
    Review
  12. Article
  13. Review
  14. Article
  15. 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.

Abigail B DiackThe Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. abigail.diack@roslin.ed.ac.uk.
James D AlibhaiNational CJD Research and Surveillance Unit, University of Edinburgh, Western General Hospital, Edinburgh EH8 9JU, UK. james.alibhai@ed.ac.uk.
Rona BarronThe Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. rona.barron@roslin.ed.ac.uk.
Barry BradfordThe Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. barry.bradford@roslin.ed.ac.uk.
Pedro PiccardoThe Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. pedro.piccardo@roslin.ed.ac.uk.
Jean C MansonThe Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. jean.manson@roslin.ed.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/J004332/1Biotechnology and Biological Sciences Research Council BBS/E/D/20251967Biotechnology and Biological Sciences Research Council BBS/E/D/20251969Medical Research Council G9721848
6 · The paper itself

Abstract

Chronic neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and prion diseases are characterised by the accumulation of abnormal conformers of a host encoded protein in the central nervous system. The process leading to neurodegeneration is still poorly defined and thus development of early intervention strategies is challenging. Unique amongst these diseases are Transmissible Spongiform Encephalopathies (TSEs) or prion diseases, which have the ability to transmit between individuals. The infectious nature of these diseases has permitted in vivo and in vitro modelling of the time course of the disease process in a highly reproducible manner, thus early events can be defined. Recent evidence has demonstrated that the cell-to-cell spread of protein aggregates by a "prion-like mechanism" is common among the protein misfolding diseases. Thus, the TSE models may provide insights into disease mechanisms and testable hypotheses for disease intervention, applicable to a number of these chronic neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAnimalsCentral Nervous SystemChronic DiseaseDisease ProgressionDisease ResistanceGene ExpressionHumansMiceMice, TransgenicNeurogliaParkinson DiseasePrion DiseasesPrionsProtein ConformationProtein FoldingPrionsneurodegenerationprionprotein misfoldingproteinopathiestransmissible spongiform encephalopathies (TSE)

Identifiers

PMID26771599
PMCPMC4730326

What OpenQuestion holds

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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.