Evidence map›Paper›PMID 29031834›Full record

ReviewFree radical biology & medicine2018

Dysregulation of neurotrophin signaling in the pathogenesis of Alzheimer disease and of Alzheimer disease in Down syndrome.

Xu-Qiao Chen, Mariko Sawa, William C Mobley

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Calcium sensor Yellow Cameleon 3.6 as a tool to support the calcium hypothesis of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Review
  11. The Nerve Growth Factor Receptor (NGFR/p75International journal of molecular sciences · 2023
    Review
  12. Article
  13. Review
  14. Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Xu-Qiao ChenUniversity of California, San Diego, La Jolla, CA 92093, United States. Electronic address: q0chen@ucsd.edu.
Mariko SawaUniversity of California, San Diego, La Jolla, CA 92093, United States.
William C MobleyUniversity of California, San Diego, La Jolla, CA 92093, United States. Electronic address: wmobley@ucsd.edu.
University of California, San Diego · US

Funding

Center for Protein Folding Machinery (RMI)PN2EY016525 · NEI · BAYLOR COLLEGE OF MEDICINE · PI CHIU, WAH · 2005 to 2015
$33.6M
Project 3: TRiC modulation of CNS pathogenesis in HD mouse modelsP01NS092525 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI THOMPSON, LESLIE MICHELS · 2016 to 2020
$6.3M
Antisense Oligonucleotides targeting APP to prevent neurodegeneration in models of Down Syndrome and Alzheimer's diseaseR01AG061151 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MOBLEY, WILLIAM C · 2019 to 2023
$3.4M
Genetic Basis of Failed Cognition in Young and Aged Mouse Models of Trisomy 21R01NS066072 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MOBLEY, WILLIAM C, YU, EUGENE · 2010 to 2014
$3.2M
Center for Protein Folding Machinery (RMI)PN1EY016525 · NEI · BAYLOR COLLEGE OF MEDICINE · PI CHIU, WAH · 2004 to 2004
$67k
NEI NIH HHS PN1 EY016525NEI NIH HHS PN2 EY016525NIA NIH HHS R01 AG061151NINDS NIH HHS P01 NS092525NINDS NIH HHS R01 NS066072
6 · The paper itself

Abstract

Neurotrophic factors, including the members of the neurotrophin family, play important roles in the development and maintenance of the nervous system. Trophic factor signals must be transmitted over long distances from axons and dendrites to the cell bodies of neurons. A mode of signaling well suited to the challenge of robust long distance signaling is the signaling endosome. We review the biology of signaling endosomes and the "signaling endosome hypothesis". Evidence for disruption of signaling endosome function in disorders of the nervous system is also reviewed. Changes in endosome structure in Alzheimer disease (AD) and Down syndrome (DS) are present early in these disorders. Data for the APP products responsible are reviewed and the consequent changes in signaling from endosomes discussed. We conclude by pointing to the need for additional studies to explore the biology of signaling endosomes in normal neurons and to elucidate their role in the pathogenesis of neurodegeneration.

Indexed as

Alzheimer DiseaseAnimalsDown SyndromeEndosomesHumansNerve Growth FactorsNerve Growth FactorsAlzheimer's diseaseAxonal transport deficitDegenerationDown syndromeEndosome enlargementNeurotrophinSignaling endosome

Identifiers

PMID29031834
PMCPMC5748266
OpenAlexW2763279643

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.