Evidence map›Paper›PMID 33048932›Full record

ArticlePLoS computational biology2020

Protein-protein interactions in neurodegenerative diseases: A conspiracy theory.

Travis B Thompson, Pavanjit Chaggar, Ellen Kuhl, Alain Goriely, Alzheimer’s Disease Neuroimaging Initiative

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A complex network perspective on brain disease.Biological reviews of the Cambridge Philosophical Society · 2026
    Review
  5. DynamicalbioRxiv : the preprint server for biology · 2026
    Article
  6. Network Diffusion Modeling in Computational Neuroscience.Advances in experimental medicine and biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Recent progress and future challenges in structure-based protein-protein interaction prediction.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Cyclin-dependent kinase 5 (CDK5) inhibitors in Parkinson disease.Journal of cellular and molecular medicine · 2024
    Review
  19. Article
  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

5 authors at 2 institutions in 2 countries.

Travis B ThompsonMathematical Institute, University of Oxford, Oxford, United Kingdom.ORCID 0000-0001-8696-4115
Pavanjit ChaggarMathematical Institute, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-8395-3047
Ellen KuhlLiving Matter Laboratory, Stanford University, Stanford, California, USA.ORCID 0000-0002-6283-935X
Alain GorielyMathematical Institute, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-6436-8483
Alzheimer’s Disease Neuroimaging Initiative
University of Oxford · GBStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases such as Alzheimer's or Parkinson's are associated with the prion-like propagation and aggregation of toxic proteins. A long standing hypothesis that amyloid-beta drives Alzheimer's disease has proven the subject of contemporary controversy; leading to new research in both the role of tau protein and its interaction with amyloid-beta. Conversely, recent work in mathematical modeling has demonstrated the relevance of nonlinear reaction-diffusion type equations to capture essential features of the disease. Such approaches have been further simplified, to network-based models, and offer researchers a powerful set of computationally tractable tools with which to investigate neurodegenerative disease dynamics. Here, we propose a novel, coupled network-based model for a two-protein system that includes an enzymatic interaction term alongside a simple model of aggregate transneuronal damage. We apply this theoretical model to test the possible interactions between tau proteins and amyloid-beta and study the resulting coupled behavior between toxic protein clearance and proteopathic phenomenology. Our analysis reveals ways in which amyloid-beta and tau proteins may conspire with each other to enhance the nucleation and propagation of different diseases, thus shedding new light on the importance of protein clearance and protein interaction mechanisms in prion-like models of neurodegenerative disease.

Indexed as

Amyloid beta-PeptidesModels, BiologicalNeurodegenerative Diseasestau ProteinsAgedAged, 80 and overBrainComputational BiologyFemaleHumansMaleAmyloid beta-Peptidestau Proteins

Identifiers

PMID33048932
PMCPMC7584458
OpenAlexW3092123400

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.