Evidence map›Paper›PMID 26338154›Full record

ReviewNature reviews. Drug discovery2015

Targeting protein aggregation for the treatment of degenerative diseases.

Yvonne S Eisele, Cecilia Monteiro, Colleen Fearns, Sandra E Encalada, R Luke Wiseman, Evan T Powers, Jeffery W Kelly

Abstract readReview
In one paragraph

Review in Nature reviews. Drug discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers.

0numbers the graph read from it
0cells of the map it votes in
175citing 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

175 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. GFP-free live neuron quantitative imaging reveals compartmentalization and growth dynamics of polyQ aggregates.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Classical and Nonclassical Nucleation Mechanisms of Biomolecules.Advances in biochemical engineering/biotechnology · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

115 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

7 authors.

Yvonne S EiseleDepartment of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA.
Cecilia MonteiroDepartment of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA.
Colleen FearnsDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
Sandra E EncaladaDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
R Luke WisemanDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
Evan T PowersDepartment of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA.
Jeffery W KellyDepartment of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA.

Funding

Probing the Biochemical Mechanisms of Amyloid DiseaseR01DK046335 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI KELLY, JEFFERY W · 1998 to 2025
$8.8M
Discovering small molecules activators of stress responsive signalingR01AG046495 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI JEFFERY W KELLY, Rockland Luke Wiseman · 2013 to 2026
$6.0M
Probing the biochemical mechanism of amyloid diseaseR37DK046335 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI KELLY, JEFFERY W · 2006 to 2015
$5.9M
Discovering Small Molecule Activators of Stress-Responsive SignalingRF1AG046495 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI KELLY, JEFFERY W, WISEMAN, ROCKLAND LUKE · 2023 to 2025
$2.8M
Modeling a cellular protein homeostasis networkR01GM101644 · NIGMS · UNIVERSITY OF MASSACHUSETTS AMHERST · PI GIERASCH, LILA M, POWERS, EVAN THOMAS · 2013 to 2016
$1.6M
BIOCHEMICAL MECHANISM OF AMYLOID DISEASER29DK046335 · NIDDK · TEXAS A&M UNIVERSITY SYSTEM · PI KELLY, JEFFERY W · 1993 to 1997
–
NIA NIH HHS AG46495NIA NIH HHS R01 AG046495NIA NIH HHS RF1 AG046495NIDDK NIH HHS DK46335NIDDK NIH HHS R01 DK046335NIDDK NIH HHS R37 DK046335NIGMS NIH HHS GM101644NIGMS NIH HHS R01 GM101644
6 · The paper itself

Abstract

The aggregation of specific proteins is hypothesized to underlie several degenerative diseases, which are collectively known as amyloid disorders. However, the mechanistic connection between the process of protein aggregation and tissue degeneration is not yet fully understood. Here, we review current and emerging strategies to ameliorate aggregation-associated degenerative disorders, with a focus on disease-modifying strategies that prevent the formation of and/or eliminate protein aggregates. Persuasive pharmacological and genetic evidence now supports protein aggregation as the cause of postmitotic tissue dysfunction or loss. However, a more detailed understanding of the factors that trigger and sustain aggregate formation and of the structure-activity relationships underlying proteotoxicity is needed to develop future disease-modifying therapies.

Indexed as

AnimalsBiological FactorsHumansNeurodegenerative DiseasesPrealbuminProtein Aggregation, PathologicalProtein FoldingProtein TransportStructure-Activity RelationshipTreatment OutcomeBiological FactorsPrealbumin

Identifiers

PMID26338154
PMCPMC4628595

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.