Cited by 87Alzheimer's disease research and treatmentsCoenzyme Q10 studies and effectsBioactive Compounds and Antitumor Agents

NAD(P)H:quinone oxidoreductase activity is increased in hippocampal pyramidal neurons of patients with alzheimer’s disease

Wang, Yunxia, Santa–Cruz, Karen, DeCarli, Charles, Johnson, Jeffrey A·2000·Neurobiology of Aging

Abstract

NAD(P)H:quinone oxidoreductase (QR) catalyzes the two-electron reduction of quinones, preventing their participation in redox cycling and subsequent generation of reactive oxygen species. Pretreatment of neuroblastoma cells with compounds, such as tert-butylhydroquinone and dimethyl fumarate, that increase QR expression protect cells from oxidative stress-induced cell death by glutamate, H(2)O(2,) and dopamine. The potential neuroprotective role of QR as well as the evidence for oxidative stress-induced neuronal cell death in Alzheimer's disease (AD) led us to examine the expression pattern of QR from AD and control patients. Histochemical staining of hippocampal sections from AD patients revealed QR activity in pyramidal neurons. The presence of QR protein in these neurons also was confirmed by immunoreactivity. In control patients, hippocampal pyramidal neurons were negative for both QR enzymatic activity and QR immunoreactivity. In addition, the QR positive neurons of AD patients were selectively located in areas where neuronal populations exhibited tau immunostaining. Our data demonstrate that QR is up-regulated in hippocampal pyramidal neurons of AD patients. We hypothesize that this is part of a neuroprotective system up-regulated in response to the AD process. Understanding this system may lead to further insights into the pathogenesis and potential new avenues of treatment for AD.

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Crossref · 10.1016/s0197-4580(00)00114-7

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  • Numerous other studies demonstrate both an increase and decrease in ARE gene expression in AD brain tissue, with an initial heightened antioxidant response due to oxidative stress followed by eventual exhaustion with decrease of ARE pathway signaling.

    “Numerous other studies demonstrate both an increase and decrease in ARE gene expression in AD brain tissue, citing an initial heightened antioxidant response due to oxidative stress [22,86,87], followed by its eventual exhaustion with the decrease of ARE pathway signaling [88].”

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Authors
Wang, Y., Santa–Cruz, K., DeCarli, C., & Johnson, J. A.
Affiliations
University of Kansas Medical Center (US)
Corresponding author
Johnson, Jeffrey A
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2000-07
Volume
21
Issue
4
Pages
525-531
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2038899025
Cited by
87
References
45
Citations by year
2025: 5 · 2024: 5 · 2023: 3 · 2022: 5 · 2021: 7 · 2020: 5 · 2019: 6 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 5 · 2014: 3 · 2013: 3 · 2012: 2
FWCI
1.43
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p30ag010182-05)
  • National Institute on Aging (AG 10182)
  • National Institute of Environmental Health Sciences (ES08089)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
Keywords
NAD(P)H:quinone oxidoreductase, Alzheimer's disease, hippocampal pyramidal neurons, oxidative stress, neuroprotection, quinone reduction, reactive oxygen species, tau protein, glutathione reductase, neurodegeneration
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Hippocampus, Humans, Blotting, Western, NAD(P)H Dehydrogenase (Quinone), tau Proteins, Cell Death, Pyramidal Cells, Oxidative Stress

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