Cited by 79Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchRedox biology and oxidative stress

Effects of oxidative and nitrosative stress in brain on p53 proapoptotic protein in amnestic mild cognitive impairment and Alzheimer disease

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Cenini, Giovanna, Sultana, Rukhsana, Memo, Maurizio, Butterfield, D. Allan·2008·Free Radical Biology and Medicine

Abstract

Many studies reported that oxidative and nitrosative stress might be important for the pathogenesis of Alzheimer's disease (AD) beginning with arguably the earliest stage of AD, i.e., as mild cognitive impairment (MCI). p53 is a proapoptotic protein that plays an important role in neuronal death, a process involved in many neurodegenerative disorders. Moreover, p53 plays a key role in the oxidative stress-dependent apoptosis. We demonstrated previously that p53 levels in brain were significantly higher in MCI and AD IPL (inferior parietal lobule) compared to control brains. In addition, we showed that in AD IPL, but not in MCI, HNE, a lipid peroxidation product, was significantly bound to p53 protein. In this report, we studied by means of immunoprecipitation analysis, the levels of markers of protein oxidation, 3-nitrotyrosine (3-NT) and protein carbonyls, in p53 in a specific region of the cerebral cortex, namely the inferior parietal lobule, in MCI and AD compared to control brains. The focus of these studies was to measure the oxidation and nitration status of this important proapoptotic protein, consistent with the hypothesis that oxidative modification of p53 could be involved in the neuronal loss observed in neurodegenerative conditions.

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Crossref · 10.1016/j.freeradbiomed.2008.03.015

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  • p53 is significantly increased in MCI and AD IPL with p53 significantly modified by protein-bound HNE, 3-NT, and carbonyls in an AD brain.

    “p53 is significantly increased in MCI and AD IPL with p53 significantly modified by protein-bound HNE, 3-NT, and carbonyls in an AD brain.”
  • p53 is significantly modified by carbonylation, but not 3NT or HNE in MCI IPL.

    “p53 is significantly modified by carbonylation, but not 3NT or HNE in MCI IPL [87,88].”

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Research works printed but not linked: 1

  1. [17]Butterfield DA, Stadman ER. Protein oxidation processes in aging brain. Adv Cell Aging Gerontol. 1997;2:161–191. [Google Scholar]

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Authors
Cenini, G., Sultana, R., Memo, M., & Butterfield, D. A.
Affiliations
  • University of Kentucky (US)
  • University of Brescia (IT)
Corresponding author
Butterfield, D. Allan
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2008-07
Volume
45
Issue
1
Pages
81-85
ISSN
0891-5849 (ISSN-L)
OpenAlex
W1989114735
Cited by
79
References
47
Citations by year
2026: 3 · 2025: 6 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 5 · 2020: 5 · 2019: 1 · 2018: 6 · 2016: 3 · 2015: 5 · 2014: 4 · 2013: 5 · 2012: 8
FWCI
5.19
Type
journal article
Language
en
Open access
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Institutional Research Information System (Università degli Studi di Brescia) (submittedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (P01AG010836, P01AG005119, R01AG029839, AG029839, AG 10836, AG0 5119)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
p53, oxidative stress, nitrosative stress, amnestic mild cognitive impairment, Alzheimer's disease, inferior parietal lobule, nitrotyrosine, protein carbonylation, lipid peroxidation, neuronal apoptosis, protein oxidation, neurodegeneration
MeSH terms
Aged, 80 and over, Alzheimer Disease, Amnesia, Brain, Cognition Disorders, Female, Humans, Male, Nitrogen, Oxidation-Reduction, Protein Binding, Tyrosine, Tumor Suppressor Protein p53, Apoptosis, Oxidative Stress

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