Evidence map›Paper›PMID 25652642›Full record

ReviewExpert opinion on therapeutic targets2015

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis.

Mythily Srinivasan, Debomoy K Lahiri

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 3% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.

  1. Pooled it
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  9. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
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  14. Differential DNA methylation in the brain as potential mediator of the association between traffic-related PMAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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28 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

2 authors at 1 institution in 1 country.

Mythily SrinivasanIndiana University School of Dentistry, Oral Pathology, Radiology and Medicine , Indianapolis, IN , USA +1 317 278 9686 ; +1 317 278 3018 ; mysriniv@iupui.edu.
Debomoy K Lahiri
Weatherford College · US

Funding

Human MicroRNA as a potential therapeutic target in Alzheimer's disease.R21AG042804 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2012 to 2013
$411k
NIA NIH HHS 1R21AG047NIA NIH HHS 5R21AG042804NIA NIH HHS R21 AG042804
6 · The paper itself

Abstract

introductionAdvances in molecular pathogenesis suggest that the chronic inflammation is a shared mechanism in the initiation and progression of multiple neurodegenerative diseases with diverse clinical manifestations such as Alzheimer's disease (AD) and Multiple sclerosis (MS). Restricted cell renewal and regenerative capacity make the neural tissues extremely vulnerable to the uncontrolled inflammatory process leading to irreversible tissue damage. AREAS COVERED: A predominant consequence of increased inflammatory signaling is the upregulation of the transcription factor, NF-κB with subsequent neuroprotective or deleterious effects depending on the strength of the signal and the type of NF-κB dimers activated. We discuss the interplay between neuroinflammation and neurodegeneration keeping in focus NF-κB signaling as the point of convergence of multiple pathways associated with the development of the neurodegenerative pathologies, AD and MS. EXPERT OPINION: Considerable interest exists in developing efficient NF-κB inhibitors for neurodegenerative diseases. The review includes an overview of natural compounds and rationally designed agents that inhibit NF-κB and mediate neuroprotection in AD and MS. The key chemical moieties of the natural and the synthetic compounds provide efficient leads for the development of effective small molecule inhibitors that selectively target NF-κB activation; this would result in the desired benefit to risk therapeutic effects.

Indexed as

Alzheimer DiseaseAnimalsDrug DesignHumansMultiple SclerosisNeuroprotective AgentsNF-kappa BSignal TransductionUp-RegulationNeuroprotective AgentsNF-kappa BAlzheimer’s diseaseamyloiddisease modifying agentsdrug targetmultiple sclerosisnatural compoundsneurodegenerationneuroinflammationNF-κBpolyphenolspromoterterpenoidstherapeutic target/mechanism

Identifiers

PMID25652642
PMCPMC5873291
OpenAlexW1973257468

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.