Cited by 1,114Alzheimer's disease research and treatmentsAntioxidant Activity and Oxidative StressDementia and Cognitive Impairment Research

Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptide

Butterfield, D.Allan, Drake, Jennifer, Pocernich, Chava, Castegna, Alessandra·2001·Trends in Molecular Medicine

Abstract

Amyloid beta-peptide (Abeta) is heavily deposited in the brains of Alzheimer's disease (AD) patients. Free-radical oxidative stress, particularly of neuronal lipids, proteins and DNA, is extensive in those AD brain areas in which Abeta is abundant. Recent research suggests that these observations might be linked, and it is postulated that Abeta-induced oxidative stress leads to neurodegeneration in AD brain. Consonant with this postulate, Abeta leads to neuronal lipid peroxidation, protein oxidation and DNA oxidation by means that are inhibited by free-radical antioxidants. Here, we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Abeta in this oxidative stress.

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Crossref · 10.1016/s1471-4914(01)02173-6

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77 of 77 references verified0 citation errors · 0 not checkable

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  • Oxidative and nitrosative stress are critical factors in the pathogenesis and progression of Alzheimer disease and amnestic mild cognitive impairment.

    “Oxidative and nitrosative stress are widely recognized as critical factors in the pathogenesis and progression of Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI).”
  • Aβ42 oligomers cause oxidative damage.

    “Aβ42 oligomers cause oxidative damage as mentioned above”
  • Aβ42 oligomers lead to synaptic dysfunction correlated with cognitive loss.

    “and these oligomers also lead to synaptic dysfunction correlated with cognitive loss [8,9,26].”
  • Brains of patients with AD exhibit prominent hallmarks of oxidative damage and decreased PRDX1 acetylation and thiol-reductive activity.

    “Brains of patients with AD exhibit prominent hallmarks of oxidative damage and decreased PRDX1 acetylation and thiol-reductive activity (47, 48) that could collectively impair GDE2 trafficking and function.”

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Authors
Butterfield, D. A., Drake, J., Pocernich, C., & Castegna, A.
Affiliations
University of Kentucky (US)
Corresponding author
Butterfield, D.Allan
Venue
Trends in Molecular Medicine
Publisher
Elsevier BV
Published
2001-12
Volume
7
Issue
12
Pages
548-554
ISSN
1471-4914 (ISSN-L)
OpenAlex
W1986384924
Cited by
1,114
References
77
Citations by year
2026: 6 · 2025: 27 · 2024: 31 · 2023: 28 · 2022: 28 · 2021: 47 · 2020: 49 · 2019: 54 · 2018: 43 · 2017: 55 · 2016: 53 · 2015: 53 · 2014: 79 · 2013: 54 · 2012: 43
FWCI
4.99
Type
journal article
Language
en
Open access
closed
Locations
  • Trends in Molecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
Funders
National Institute on Aging (P01AG010836, P01AG005119, AG 10836, AG12423, AG0 5119, R01AG012423)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, amyloid-beta, oxidative stress, lipid peroxidation, phospholipid peroxidation, protein oxidation, DNA oxidation, free radicals, antioxidants, neurodegeneration, brain
MeSH terms
Alzheimer Disease, Brain, DNA, Free Radicals, Humans, Nerve Tissue Proteins, RNA, Lipid Peroxidation, Amyloid beta-Peptides, Oxidative Stress

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