Evidence map›Paper›PMID 26281945›Full record

ReviewFree radical biology & medicine2015

Nrf2--a therapeutic target for the treatment of neurodegenerative diseases.

Delinda A Johnson, Jeffrey A Johnson

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 5 pooled it
16.1field-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

198 citing papers in PubMed, 5 syntheses or guidelines pooled it, 315 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Review
  8. Review
  9. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Molecular Insights of Neuroprotective Effect ofInternational journal of molecular sciences · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Coenzyme Q10 and Intracellular Signalling Pathways: Clinical Relevance.International journal of molecular sciences · 2025
    Review
  18. Article
  19. Review
  20. Article

138 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.

Delinda A JohnsonSchool of Pharmacy, University of Wisconsin-Madison, Madison, WI 53705, USA. Electronic address: dajohnson@pharmacy.wisc.edu.
Jeffrey A JohnsonSchool of Pharmacy, University of Wisconsin-Madison, Madison, WI 53705, USA. Electronic address: jajohnson@pharmacy.wisc.edu.
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
Tranthyretin's Regulatory Role in Beta-Amyloid Aggregation and ToxicityR01AG033493 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI JOHNSON, JEFFREY A, MURPHY, REGINA M. · 2009 to 2016
$2.7M
NIA NIH HHS P50 AG033514NIA NIH HHS P50AG033514NIA NIH HHS R01 AG033493NIEHS NIH HHS R01 ES008089NIEHS NIH HHS R01 ES010042NIEHS NIH HHS R01 ES08089NIEHS NIH HHS R01 ES10042
6 · The paper itself

Abstract

The brain is very sensitive to changes in redox status; thus maintaining redox homeostasis in the brain is critical for the prevention of accumulating oxidative damage. Aging is the primary risk factor for developing neurodegenerative diseases. In addition to age, genetic and environmental risk factors have also been associated with disease development. The primary reactive insults associated with the aging process are a result of oxidative stress (OS) and nitrosative stress (NS). Markers of increased oxidative stress, protein and DNA modification, inflammation, and dysfunctional proteostasis have all been implicated in contributing to the progression of neurodegeneration. The ability of the cell to combat OS/NS and maintain a clearance mechanism for misfolded aggregating proteins determines whether or not it will survive. A critical pathway in this regard is the Nrf2 (nuclear factor erythroid 2-related factor 2)- antioxidant response element (ARE) pathway. Nrf2 activation has been shown to mitigate a number of pathologic mechanisms associated with Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. This review will focus on the role of Nrf2 in these diseases and the potential for Nrf2 activation to attenuate disease progression.

Indexed as

AnimalsBrainHumansNeurodegenerative DiseasesNF-E2-Related Factor 2Oxidation-ReductionOxidative StressSignal TransductionNF-E2-Related Factor 2Alzheimer’s diseaseAmyotrophic lateral sclerosisHuntington’s diseaseMultiple sclerosisNrf2Oxidative stressParkinson’s disease

Identifiers

PMID26281945
PMCPMC4809057
OpenAlexW1166587220

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.