Evidence map›Paper›PMID 26109945›Full record

ReviewNeural regeneration research2015

The p75 neurotrophin receptor: at the crossroad of neural repair and death.

Rick B Meeker, Kimberly S Williams

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

120 citing papers in PubMed, 190 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. A lifespan staging model of basal forebrain cholinergic vulnerability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. p75Bone reports · 2025
    Article
  16. P75iScience · 2025
    Article
  17. Review
  18. Review
  19. Article
  20. Article

60 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

2 authors at 1 institution in 1 country.

Rick B MeekerDepartment of Neurology, University of North Carolina, Chapel Hill, NC, USA.
Kimberly S WilliamsCurriculum in Neurobiology, University of North Carolina, Chapel Hill, NC, USA.
University of North Carolina at Chapel Hill · US

Funding

Neurotrophin mimetic therapeutics for HIV-associated neural dysfunctionR01MH085606 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MEEKER, RICK B · 2009 to 2013
$1.7M
Neurotrophin Protection in HIV and AgingR01NS083164 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MEEKER, RICK B · 2013 to 2016
$1.1M
Neurotrophin- Chemokine Receptor Interactions Regulate Macrophage ActivationF31MH101019 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIAMS, KIMBERLY S. · 2013 to 2014
$65k
NIMH NIH HHS F31 MH101019NIMH NIH HHS R01 MH085606NINDS NIH HHS R01 NS083164
6 · The paper itself

Abstract

The strong repair and pro-survival functions of neurotrophins at their primary receptors, TrkA, TrkB and TrkC, have made them attractive candidates for treatment of nervous system injury and disease. However, difficulties with the clinical implementation of neurotrophin therapies have prompted the search for treatments that are stable, easier to deliver and allow more precise regulation of neurotrophin actions. Recently, the p75 neurotrophin receptor (p75(NTR)) has emerged as a potential target for pharmacological control of neurotrophin activity, supported in part by studies demonstrating 1) regulation of neural plasticity in the mature nervous system, 2) promotion of adult neurogenesis and 3) increased expression in neurons, macrophages, microglia, astrocytes and/or Schwann cells in response to injury and neurodegenerative diseases. Although the receptor has no intrinsic catalytic activity it interacts with and modulates the function of TrkA, TrkB, and TrkC, as well as sortilin and the Nogo receptor. This provides substantial cellular and molecular diversity for regulation of neuron survival, neurogenesis, immune responses and processes that support neural function. Upregulation of the p75(NTR) under pathological conditions places the receptor in a key position to control numerous processes necessary for nervous system recovery. Support for this possibility has come from recent studies showing that small, non-peptide p75(NTR) ligands can selectively modify pro-survival and repair functions. While a great deal remains to be discovered about the wide ranging functions of the p75(NTR), studies summarized in this review highlight the immense potential for development of novel neuroprotective and neurorestorative therapies.

Indexed as

braininjurymicroglianeural progenitorneurodegenerative diseaseneuronplasticitytherapy

Identifiers

PMID26109945
PMCPMC4468762
OpenAlexW1960312392

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.