Evidence map›Paper›PMID 36012242›Full record

ReviewInternational journal of molecular sciences2022

The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer's Disease.

Emily Sun, Aishat Motolani, Leonardo Campos, Tao Lu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 3 pooled it
37.5field-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

190 citing papers in PubMed, 3 syntheses or guidelines pooled it, 330 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Role of aging‑related cytokines in neurodegenerative disease (Review).International journal of molecular medicine · 2026
    Review
  17. Protective Effects of a Propolis-Journal of microbiology and biotechnology · 2026
    Article
  18. Article
  19. Article
  20. Article

130 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

4 authors at 2 institutions in 1 country.

Emily SunDepartment of Pharmacology & Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Aishat MotolaniDepartment of Pharmacology & Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Leonardo CamposDepartment of Biological Sciences, Columbia University, 70 Morning Drive, New York, NY 10027, USA.
Tao LuDepartment of Pharmacology & Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.ORCID 0000-0002-0013-4987
Indiana University School of MedicineColumbia University · US

Funding

Gene-specific responses to NF-kB through lysine and arginine methylation of p65R01GM120156 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI LU, TAO · 2017 to 2021
$1.5M
NIGMS NIH HHS 1R01GM120156-01A1NIGMS NIH HHS R01 GM120156
6 · The paper itself

Abstract

Alzheimer's Disease (AD) is the most common neurodegenerative disease worldwide, with a high prevalence that is expected to double every 20 years. Besides the formation of Aβ plaques and neurofibrillary tangles, neuroinflammation is one the major phenotypes that worsens AD progression. Indeed, the nuclear factor-κB (NF-κB) is a well-established inflammatory transcription factor that fuels neurodegeneration. Thus, in this review, we provide an overview of the NF-κB role in the pathogenesis of AD, including its interaction with various molecular factors in AD mice models, neurons, and glial cells. Some of these cell types and molecules include reactive microglia and astrocytes, β-secretase, APOE, glutamate, miRNA, and tau protein, among others. Due to the multifactorial nature of AD development and the failure of many drugs designed to dampen AD progression, the pursuit of novel targets for AD therapeutics, including the NF-κB signaling pathway, is rising. Herein, we provide a synopsis of the drug development landscape for AD treatment, offering the perspective that NF-κB inhibitors may generate widespread interest in AD research in the future. Ultimately, the additional investigation of compounds and small molecules that target NF-κB signaling and the complete understanding of NF-κB mechanistic activation in different cell types will broaden and provide more therapeutic options for AD patients.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesNF-kappa BAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsHumansMiceMicrogliaAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesNF-kappa BAlzheimer’sdrug discoveryinflammationneurodegenerationNF-κB

Identifiers

PMID36012242
PMCPMC9408758
OpenAlexW4291000683

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.