Evidence map›Paper›PMID 17107602›Full record

ReviewBrain pathology (Zurich, Switzerland)2006

Pathophysiological mechanisms for actions of the neurotrophins.

Jeffery L Twiss, Jay H Chang, N Carolyn Schanen

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. [Research progress of P75 neurotrophin receptor and new idea of nonunion treatment].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2017
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. p75 neurotrophin receptor regulates agonist-induced pulmonary vasoconstriction.American journal of physiology. Heart and circulatory physiology · 2008
    Article
  19. Article
  20. Review
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.

Jeffery L TwissNemours Biomedical Research, Alfred I. duPont Hospital for Children, Wilmington, Delaware 19803, USA. twiss@medsci.udel.edu
Jay H Chang
N Carolyn Schanen
Alfred I. duPont Hospital for Children · US

Funding

Translation during Nerve RegenerationR01NS041596 · NINDS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI TWISS, JEFFERY L · 2001 to 2018
$4.0M
TARGETED INVESTIGATION OF DISTAL XQ IN RETT SYNDROMER01HD037874 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SCHANEN, N. CAROLYN · 2000 to 2010
$2.3M
Regulation of intra-axonal protein systhesisR01NS049041 · NINDS · NEMOURS CHILDREN'S HOSPITAL, DELAWARE · PI TWISS, JEFFERY L · 2006 to 2009
$1.2M
NICHD NIH HHS R01 HD037874NICHD NIH HHS R01-HD037874NINDS NIH HHS R01 NS041596NINDS NIH HHS R01-NS041596NINDS NIH HHS R01 NS049041NINDS NIH HHS R01-NS049041
6 · The paper itself

Abstract

Neurotrophins provide trophic and tropic support for different neuronal subpopulations in the developing and adult nervous systems. Expression of the neurotrophins and their receptors can be altered in several different disease or injury states that impact upon the functions in the central and peripheral nervous systems. The intracellular signals used by the neurotrophins are triggered by ligand binding to the cell surface Trk and p75NTR receptors. In general, signals emanating from Trk receptors support survival, growth and synaptic strengthening, while those emanating from p75NTR induce apoptosis, attenuate growth and weaken synaptic signaling. Mature neurotrophins are the preferred ligand for Trk proteins while p75NTR binds preferentially to the proneurotrophins and serves as a signaling component of the receptor complex for growth inhibitory molecules of central nervous system myelin [ie, myelin-associated glycoprotein (MAG), oligodendrocyte-myelin glycoprotein (OMgP) and Nogo]. The functional antagonism between Trk and p75NTR signaling may significantly impact the pathogenesis of human neurodevelopmental and neurodegenerative diseases and further complicate therapeutic uses of exogenous neurotrophins. The potential for each is discussed in this review.

Indexed as

AnimalsHumansNerve Growth FactorsNerve RegenerationNervous System DiseasesNeuronal PlasticityNeuronsReceptors, Nerve Growth FactorSignal TransductionNerve Growth FactorsReceptors, Nerve Growth Factor

Identifiers

PMID17107602
PMCPMC8095803
OpenAlexW2118448920

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.