Evidence map›Paper›PMID 25805130›Full record

ArticleDevelopmental cell2015

Proteostatic hotspots in amyloid fibrils protect us from neurodegeneration.

Jay Kumar Singh, William E Balch

Abstract readComment
PubMed Publisher
In one paragraph

Article in Developmental cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Aducanumab binding to AβProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Article
  3. Article
  4. Current and future treatment of amyloid diseases.Journal of internal medicine · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Jay Kumar SinghThe Scripps Research Institute, La Jolla, CA 92037, USA.
William E BalchThe Scripps Research Institute, La Jolla, CA 92037, USA. Electronic address: webalch@scripps.edu.

Funding

Restoration of mutant CFTR stability and functionR01DK051870 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BALCH, WILLIAM EDWARD · 1996 to 2020
$8.7M
6 · The paper itself

Abstract

Alzheimer's disease remains a formidable challenge for therapeutic management. In a recent report in Nature Structural and Molecular Biology, Cohen et al. (2015) present intriguing results showing that "designer" molecular chaperones may hold the key to an evolutionarily conserved program for management of toxic oligomer species contributing to brain pathobiology.

Indexed as

Protein Aggregation, PathologicalAmyloid beta-PeptidesAnimalsFemaleHumansMaleMolecular ChaperonesAmyloid beta-PeptidesMolecular Chaperones

Identifiers

What OpenQuestion holds

Textmetadata
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.