Evidence map›Paper›PMID 25258700›Full record

ArticleJournal of Alzheimer's disease & Parkinsonism2013

Chaperone-dependent Neurodegeneration: A Molecular Perspective on Therapeutic Intervention.

Aaron Carman, Sarah Kishinevsky, John Koren, Wenjie Lou, Gabriela Chiosis

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease & Parkinsonism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Radiosynthesis and preclinical evaluation of [EJNMMI radiopharmacy and chemistry · 2023
    Article
  10. Review
  11. Review
  12. Review
  13. Neurobiological Opportunities in Diabetic Polyneuropathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. 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.

Aaron CarmanDepartment of Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Centre, New York, NY, USA.
Sarah KishinevskyDepartment of Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Centre, New York, NY, USA.
John KorenDepartment of Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Centre, New York, NY, USA.
Wenjie LouDepartment of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY, USA.
Gabriela ChiosisDepartment of Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Centre, New York, NY, USA.

Funding

Small molecule Hsp90 inhibitors in AD treatmentU01AG032969 · NIA · SLOAN-KETTERING INST CAN RESEARCH · PI CHIOSIS, GABRIELA · 2010 to 2014
$3.5M
Biomarkers for predicting response to Hsp90 therapyR01CA172546 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI CHIOSIS, GABRIELA, DUNPHY, MARK P. · 2013 to 2017
$2.9M
Hsp90 inhibitors as suppressors of protein misfolding toxicityR21AG028811 · NIA · SLOAN-KETTERING INST CAN RESEARCH · PI CHIOSIS, GABRIELA · 2007 to 2008
$406k
NCI NIH HHS R01 CA172546NIA NIH HHS R21 AG028811NIA NIH HHS U01 AG032969
6 · The paper itself

Abstract

Maintenance of cellular homeostasis is regulated by the molecular chaperones. Under pathogenic conditions, aberrant proteins are triaged by the chaperone network. These aberrant proteins, known as "clients," have major roles in the pathogenesis of numerous neurological disorders, including tau in Alzheimer's disease, α-synuclein and LRRK2 in Parkinson's disease, SOD-1, TDP-43 and FUS in amyotrophic lateral sclerosis, and polyQ-expanded proteins such as huntingtin in Huntington's disease. Recent work has demonstrated that the use of chemical compounds which inhibit the activity of molecular chaperones subsequently alter the fate of aberrant clients. Inhibition of Hsp90 and Hsc70, two major molecular chaperones, has led to a greater understanding of how chaperone triage decisions are made and how perturbing the chaperone system can promote clearance of these pathogenic clients. Described here are major pathways and components of several prominent neurological disorders. Also discussed is how treatment with chaperone inhibitors, predominately Hsp90 inhibitors which are selective for a diseased state, can relieve the burden of aberrant client signaling in these neurological disorders.

Indexed as

Aberrant neurological proteinsChaperone inhibitorsMolecular chaperonesNeurodegeneration

Identifiers

PMID25258700
PMCPMC4172285

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.