Evidence map›Paper›PMID 27697064›Full record

ReviewCurrent Alzheimer research2017

Targeting Tumor Necrosis Factor Alpha for Alzheimer's Disease.

Boris Decourt, Debomoy K Lahiri, Marwan N Sabbagh

Open access · greenAbstract readReview
In one paragraph

Review in Current Alzheimer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 6 pooled it
9.5field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 6 syntheses or guidelines pooled it, 368 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
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  6. Pooled it
  7. Circulating Mediators of Apoptosis and Inflammation in Aging; Physical Exercise Intervention.International journal of environmental research and public health · 2021
    Trial
  8. Trial
  9. Neurobehavioral Consequences of Obesity: The Role of Inflammation.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Plasma inflammatory biomarker profiles across the Alzheimer's disease spectrum in the Bio-Hermes cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

136 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

3 authors at 3 institutions in 1 country.

Boris DecourtBanner Sun Health Research Institute, 10515 W. Santa Fe Dr., Sun City AZ 85351, United States.
Debomoy K LahiriInstitute of Psychiatry Research, Department of Psychiatry, School of Medicine, Indiana University-Purdue University, Indianapolis, IN, United States.
Marwan N SabbaghAlzheimer's and Memory Disorders Division, Barrow Neurological Institute, 240 West Thomas, Ste 301, Phoenix, AZ 85013, United States.
Banner Sun Health Research Institute · USBarrow Neurological Institute · USIndiana University – Purdue University Indianapolis · US

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI REIMAN, ERIC MICHAEL · 2001 to 2020
$32.5M
Neurobiological Role of MicroRNA in Alzheimer'sR01AG051086 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2015 to 2019
$1.9M
Pre-clinical testing of lenalidomide as pleiotropic therapeutics of Alzheimer's diseaseK01AG047279 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI DECOURT, BORIS · 2015 to 2019
$534k
NIA NIH HHS K01 AG047279NIA NIH HHS P30 AG019610NIA NIH HHS R01 AG051086
6 · The paper itself

Abstract

Alzheimer's disease (AD) affects an estimated 44 million individuals worldwide, yet no therapeutic intervention is available to stop the progression of the dementia. Neuropathological hallmarks of AD are extracellular deposits of amyloid beta (Aβ) peptides assembled in plaques, intraneuronal accumulation of hyperphosphorylated tau protein forming tangles, and chronic inflammation. A pivotal molecule in inflammation is the pro-inflammatory cytokine TNF-α. Several lines of evidence using genetic and pharmacological manipulations indicate that TNF-α signaling exacerbates both Aβ and tau pathologies in vivo. Interestingly, preventive and intervention anti-inflammatory strategies demonstrated a reduction in brain pathology and an amelioration of cognitive function in rodent models of AD. Phase I and IIa clinical trials suggest that TNF-α inhibitors might slow down cognitive decline and improve daily activities in AD patients. In the present review, we summarize the evidence pointing towards a beneficial role of anti-TNF-α therapies to prevent or slow the progression of AD. We also present possible physical and pharmacological interventions to modulate TNF-α signaling in AD subjects along with their limitations.

Indexed as

Alzheimer DiseaseAnimalsAnti-Inflammatory AgentsHumansTumor Necrosis Factor-alphaAnti-Inflammatory AgentsTumor Necrosis Factor-alphaAlzheimer's diseaseBACE1etanerceptinflammationneuroinflammationthalidomideTNF-alpha.

Identifiers

PMID27697064
PMCPMC5328927
OpenAlexW2532720480

What OpenQuestion holds

Textmetadata
LicenceTDM
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.