Evidence map›Paper›PMID 30778285›Full record

ArticleFrontiers in neuroscience2019

Targeting TNFR2 as a Novel Therapeutic Strategy for Alzheimer's Disease.

Natalia Ortí-Casañ, Yingying Wu, Petrus J W Naudé, Peter P De Deyn, Inge S Zuhorn, Ulrich L M Eisel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 76 citations in OpenAlex.

  1. Inflammation profiles in Alzheimer's disease relate to cognition and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  9. Unraveling the Immune Puzzle: Role of Immunomodulation in Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Cerebrospinal fluid levels of tumour necrosis factor-Frontiers in aging neuroscience · 2025
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
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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

6 authors at 2 institutions in 1 country.

Natalia Ortí-CasañDepartment of Molecular Neurobiology, Groningen Institute for Evolutionary Life Sciences, Faculty of Science and Engineering, University of Groningen, Groningen, Netherlands.
Yingying WuDepartment of Molecular Neurobiology, Groningen Institute for Evolutionary Life Sciences, Faculty of Science and Engineering, University of Groningen, Groningen, Netherlands.
Petrus J W NaudéDepartment of Molecular Neurobiology, Groningen Institute for Evolutionary Life Sciences, Faculty of Science and Engineering, University of Groningen, Groningen, Netherlands.
Peter P De DeynDepartment of Neurology and Alzheimer Center, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
Inge S ZuhornDepartment of Biomedical Engineering, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
Ulrich L M EiselDepartment of Molecular Neurobiology, Groningen Institute for Evolutionary Life Sciences, Faculty of Science and Engineering, University of Groningen, Groningen, Netherlands.
University of Groningen · NLUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. Accumulating experimental evidence shows the important linkage between tumor necrosis factor-α (TNF) and AD, but the exact role of TNF in AD is still not completely understood. Although TNF-inhibitors are successfully used for treating several diseases, total inhibition of TNF can cause side effects, particularly in neurological diseases. This is attributed to the opposing roles of the two TNF receptors. TNF receptor 1 (TNFR1) predominantly mediates inflammatory and pro-apoptotic signaling pathways, whereas TNF receptor 2 (TNFR2) is neuroprotective and promotes tissue regeneration. Therefore, the specific activation of TNFR2 signaling, either by directly targeting TNFR2 via TNFR2 agonists or by blocking TNFR1 signaling with TNFR1-selective antagonists, seems a promising strategy for AD therapy. This mini-review discusses the involvement of TNFR2 and its signaling pathway in AD and outlines its potential application as therapeutic target. A better understanding of the function of TNFR2 may lead to the development of a treatment for AD.

Indexed as

agonistsAlzheimer’s diseaseantagonistsneurodegenerationneuroprotectiontumor necrosis factor

Identifiers

PMID30778285
PMCPMC6369349
OpenAlexW2911840604

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.