Evidence map›Paper›PMID 22742419›Full record

ReviewRecent patents on CNS drug discovery2012

The Nrf2-ARE pathway: a valuable therapeutic target for the treatment of neurodegenerative diseases.

Gururaj Joshi, Jeffrey A Johnson

Open access · bronzeAbstract readReview
In one paragraph

Review in Recent patents on CNS drug discovery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
6.3field-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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

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  14. AIMS neuroscience · 2024
    Article
  15. A dicer-related helicase opposes the age-related pathology from SKN-1 activation in ASI neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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55 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.

Gururaj JoshiDivision of Pharmaceutical Sciences, School of Pharmacy, 6125 Rennebohm Hall, 777 Highland Avenue, University of Wisconsin, Madison, WI 53705, USA.
Jeffrey A Johnson
University of Wisconsin–Madison · US

Funding

Wisconsin Alzheimer's Disease Research CenterP50AG033514 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI CHAPPELL, RICHARD J · 2009 to 2018
$16.2M
The Nrf2-ARE pathway in modulating Parkinson's DiseaseR01ES010042 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI JOHNSON, JEFFREY A · 2001 to 2010
$4.0M
Transcriptional Control of Antioxidant Genes in BrainR01ES008089 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI JOHNSON, JEFFREY A · 2002 to 2013
$3.7M
BRAIN GLUTATHIONE S-TRANSFERASES AND NEUROTOXICITYR29ES008089 · NIEHS · UNIVERSITY OF WISCONSIN MADISON · PI JOHNSON, JEFFREY A · 1996 to 2000
$104k
NIA NIH HHS P50 AG033514NIEHS NIH HHS ES08089NIEHS NIH HHS ES10042NIEHS NIH HHS R01 ES008089NIEHS NIH HHS R01 ES010042NIEHS NIH HHS R29 ES008089
6 · The paper itself

Abstract

Modulation of NF-E2 related factor 2 (Nrf2) has been shown in several neurodegenerative disorders. The overexpression of Nrf2 has become a potential therapeutic avenue for various neurodegenerative disorders such as Parkinson, Amyotrophic lateral sclerosis, and Alzheimer's disease. The expression of phase II detoxification enzymes is governed by the cis-acting regulatory element known as antioxidant response element (ARE). The transcription factor Nrf2 binds to ARE thereby transcribing multitude of antioxidant genes. Keap1, a culin 3-based E3 ligase that targets Nrf2 for degradation, sequesters Nrf2 in cytoplasm. Disruption of Keap1-Nrf2 interaction or genetic overexpression of Nrf2 can increase the endogenous antioxidant capacity of the brain thereby rendering protection against oxidative stress in neurodegenerative disorders. This review primarily focuses on recent patents that target Nrf2 overexpression as a promising therapeutic strategy for the treatment of neurodegenerative disorders.

Indexed as

Molecular Targeted TherapyAnimalsAntioxidant Response ElementsBrainDrugs, InvestigationalHumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1Nerve Tissue ProteinsNeurodegenerative DiseasesNeuronsNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressPatents as TopicSignal TransductionDrugs, InvestigationalIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Nerve Tissue ProteinsNeuroprotective AgentsNFE2L2 protein, humanNF-E2-Related Factor 2

Identifiers

PMID22742419
PMCPMC3625035
OpenAlexW2066922594

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.