Evidence map›Paper›PMID 25342942›Full record

ArticleCurrent neuropharmacology2014

Noradrenergic regulation of glial activation: molecular mechanisms and therapeutic implications.

David Braun, Jose L M Madrigal, Douglas L Feinstein

Open access · bronzeAbstract read
In one paragraph

Article in Current neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Locus coeruleus-entorhinal cortex tract integrity is linked to plasma tau and glial fibrillary acidic protein.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  4. Article
  5. Review
  6. International journal of molecular sciences · 2024
    Article
  7. Article
  8. Article
  9. Multisensory Stimulation Reverses Memory Impairment in AdrβInternational journal of molecular sciences · 2023
    Article
  10. Review
  11. Article
  12. Noradrenaline in Alzheimer's Disease: A New Potential Therapeutic Target.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Astrocytic cAMP Pathway in Health and Disease.International journal of molecular sciences · 2019
    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 2 institutions in 2 countries.

David BraunDepartment of Anesthesiology, University of Illinois at Chicago, Chicago IL, USA, 60612.
Jose L M MadrigalDepartamento de Farmacología, Universidad Complutense de Madrid, Spain.
Douglas L FeinsteinDepartment of Anesthesiology, University of Illinois at Chicago, Chicago IL, USA, 60612 ; Jesse Brown VA Medical Center, Chicago IL, USA, 60612.
University of Illinois Chicago · USUniversidad Complutense de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been known for many years that the endogenous neurotransmitter noradrenaline (NA) exerts anti-inflammatory and neuroprotective effects both in vitro and in vivo. In many cases the site of action of NA are beta-adrenergic receptors (βARs), causing an increase in intracellular levels of cAMP which initiates a broad cascade of events including suppression of inflammatory transcription factor activities, alterations in nuclear localization of proteins, and induction of patterns of gene expression mediated through activity of the CREB transcription factor. These changes lead not only to reduced inflammatory events, but also contribute to neuroprotective actions of NA by increasing expression of neurotrophic substances including BDNF, GDNF, and NGF. These properties have prompted studies to determine if treatments with drugs to raise CNS NA levels could provide benefit in various neurological conditions and diseases having an inflammatory component. Moreover, increasing evidence shows that disruptions in endogenous NA levels occurs in several diseases and conditions including Alzheimer's disease (AD), Parkinson's disease (PD), Down's syndrome, posttraumatic stress disorder (PTSD), and multiple sclerosis (MS), suggesting that damage to NA producing neurons is a common factor that contributes to the initiation or progression of neuropathology. Methods to increase NA levels, or to reduce damage to noradrenergic neurons, therefore represent potential preventative as well as therapeutic approaches to disease.

Indexed as

Alzheimer’s diseaseamyloidEAEGFAPlocus coeruleusmultiple sclerosisnoradrenalinereviewtransgenic micetyrosine hydroxylase.

Identifiers

PMID25342942
PMCPMC4207074
OpenAlexW2006750659

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.