Evidence map›Paper›PMID 12476354›Full record

ReviewJournal of neurovirology2002

Tumor necrosis factor-alpha in normal and diseased brain: Conflicting effects via intraneuronal receptor crosstalk?

Seth W Perry, Stephen Dewhurst, Matthew J Bellizzi, Harris A Gelbard

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neurovirology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
  2. Article
  3. Ex-VivoJournal of proteome research · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Crosstalk between anticancer drugs and mitochondrial functions.Current research in pharmacology and drug discovery · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Polymorphic Variants ofMediators of inflammation · 2018
    Article
  17. Article
  18. Article
  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

4 authors at 1 institution in 1 country.

Seth W PerryCenter for Aging and Developmental Biology, Aab Biomedical Institute, and the Departments of Neurology, University of Rochester Medical Center, Rochester, New York, USA. Seth_Perry@urmc.rochester.edu
Stephen Dewhurst
Matthew J Bellizzi
Harris A Gelbard
University of Rochester Medical Center · US

Funding

Targeted Neuro Protection of HIV-1 Associated Neurologic DiseaseP01MH064570 · NIMH · UNIVERSITY OF ROCHESTER · PI GELBARD, HARRIS A · 2001 to 2014
$19.4M
University of Rochester Mentoring Environment: Nurturing Training Opportunities in Research (UR-MENTOR)T32GM007356 · NIGMS · UNIVERSITY OF ROCHESTER · PI O'BANION, M. KERRY · 1985 to 2023
$15.1M
ROLE OF PAF IN HIV-1 NEUROPATHOGENESISR01MH056838 · NIMH · UNIVERSITY OF ROCHESTER · PI GELBARD, HARRIS A · 1996 to 2014
$5.2M
Training in HIV Replication and PathogenesisT32AI049815 · NIAID · UNIVERSITY OF ROCHESTER · PI WEDEKIND, JOSEPH E · 2001 to 2020
$3.5M
NIAID NIH HHS T32 AI049815NIAID NIH HHS T32 AI49815NIGMS NIH HHS T32 GM007356NIGMS NIH HHS T32 GM07356NIMH NIH HHS P01 MH064570NIMH NIH HHS P01 MH64570NIMH NIH HHS R01 MH056838NIMH NIH HHS R01 MH56838
6 · The paper itself

Abstract

Tumor necrosis factor-alpha (TNF-alpha) is pleiotropic mediator of a diverse array of physiological and neurological functions, including both normal regulatory functions and immune responses to infectious agents. Its role in the nervous system is prominent but paradoxical. Studies on uninflamed or "normal" brain have generally attributed TNF-alpha a neuromodulatory effect. In contrast, in inflamed or diseased brain, the abundance of evidence suggests that TNF-alpha has an overall neurotoxic effect, which may be particularly pronounced for virally mediated neurological disease. Still others have found TNF-alpha to be protective under some conditions of neurological insult. It is still uncertain exactly how TNF-alpha is able to induce these opposing effects through receptor activation of only a limited set of cell signaling pathways. In this paper, we provide support from the literature to advance our hypothesis that one mechanism by which TNF-alpha can exert its paradoxical effects in the brain is via crosstalk with signaling pathways of growth factors or other cytokines.

Indexed as

BrainBrain DiseasesHumansNeuronsReceptor Cross-TalkTumor Necrosis Factor-alphaTumor Necrosis Factor-alpha

Identifiers

PMID12476354
PMCPMC7094979
OpenAlexW2136509648

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.