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Cited by 120Redox biology and oxidative stressAlzheimer's disease research and treatmentsBioactive Compounds and Antitumor Agents

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

Quinone reductase (NQO1), a sensitive redox indicator, is increased in Alzheimer’s disease

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Raina, A.K., Templeton, D.J., deak, J.C., Perry, G., Smith, M.A.·1999·Redox Report
DOI 10.1179/135100099101534701
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Abstract

NAD(P)H:quinone oxidoreductase 1 (NQO1), a redox-regulated flavoenzyme, plays a central role in monitoring cellular redox state. NQO1 acts to protect against oxidative stress induced by a variety of metabolic situations, including metabolism of quinones and other xenobiotics, by: (i) functioning as a two electron donor to provide a shunt that competes with the formation of reactive oxygen species; (ii) maintaining reduced coenzyme Q; and (iii) regulating the stress activated kinase pathway. In Alzheimer's disease, while there is abundant evidence for the involvement of oxidative stress, the cause or the consequences are largely unresolved. We suspected that increased NQO1 could signal a major shift in redox balance in Alzheimer's disease and, in this study, found that NQO1 is localized not only to neurofibrillary tangles but also the cytoplasm of hippocampal neurons. By marked contrast, there is very little NQO1 in the same neuronal populations in young and age-matched controls. This novel association of NQO1 further buttresses the nexus of oxidative stress, via free radicals, with selective neuronal vulnerability and also supports a fundamental abnormality in redox balance in Alzheimer's disease.

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Research works printed but not linked: 7

  1. Smith MA, 1998, Alzheimer disease, 1
  2. Smith MA, 1994, Am J Pathol, 145, 42
  3. Furuta A, 1995, Am J Pathol, 146, 357
  4. Sternberger LA.Immunocytochemistg. New York: Wiley, 1986.
  5. Ernster L, 1992, Biofactors, 3, 241
  6. Ernster L, 1994, Ubiquinol as a biological antioxidant: a review, 185
  7. Pappolla MA, 1992, Am J Pathol, 140, 621

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Metadata

Authors
Raina, A. K., Templeton, D. J., deak, J. C., Perry, G., & Smith, M. A.
Affiliations
Case Western Reserve University (US)
ORCID
Venue
Redox Report
Publisher
Informa UK Limited
Published
1999-02
Volume
4
Issue
1-2
Pages
23-27
ISSN
  • 1351-0002 (ISSN-L)
  • 1743-2928
DOI
10.1179/135100099101534701
OpenAlex
W1972676451
Cited by
120
References
38
Citations by year
2025: 3 · 2024: 4 · 2023: 2 · 2022: 7 · 2021: 6 · 2020: 10 · 2019: 8 · 2018: 2 · 2017: 6 · 2016: 4 · 2015: 4 · 2014: 5 · 2013: 5 · 2012: 3
FWCI
1.50
Type
journal article
Language
en
Open access
Locations
  • Redox Report (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Alzheimer's Association
  • American Health Assistance Foundation
  • National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
Keywords
NQO1, NAD(P)H:quinone oxidoreductase 1, Alzheimer's disease, oxidative stress, redox homeostasis, flavoenzyme, neurofibrillary tangles, hippocampal neurons, reactive oxygen species, neuronal vulnerability
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Humans, Quinone Reductases, Oxidative Stress

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