Cited by 896Alzheimer's disease research and treatmentsRedox biology and oxidative stressDementia and Cognitive Impairment Research

Oxidative stress in Alzheimer’s disease

Open access
Smith, Mark A., Rottkamp, Catherine A., Nunomura, Akihiko, Raina, Arun K., Perry, George·2000·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Abstract

Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer's disease. Examination of Alzheimer's disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons. While this suggests that oxidative stress is a proximal event in Alzheimer's disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-beta-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer's disease pathogenesis and novel therapeutic approaches.

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Crossref · 10.1016/s0925-4439(00)00040-5

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  • Oxidative damage has been implicated in all major neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis.

    “Oxidative damage has been implicated in all major neurodegenerative diseases including Alzheimer’s disease (AD) [108,109], Parkinson’s disease (PD) [110,111], Huntington’s disease (HD) [112,113], amyotrophic lateral sclerosis (ALS) [114], and multiple sclerosis (MS) [115].”
  • Protein oxidation, nucleic acid oxidation, and lipid peroxidation are markers of oxidative stress described as early alterations in the Alzheimer's disease brain, supporting the oxidative stress hypothesis of AD pathogenesis.

    “All of these markers of OS have been described as an early alteration in the AD brain, and this concept has been used in the past to support the ‘oxidative stress hypothesis’ in the pathogenesis of AD [20,28,29,30].”

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Cites

1 retracted

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Research works printed but not linked: 3

  1. Good, 1996, Am. J. Pathol., 149, 21
  2. Montine, 1996, Am. J. Pathol., 148, 89
  3. Cras, 1990, Am. J. Pathol., 137, 241

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Authors
Smith, M. A., Rottkamp, C. A., Nunomura, A., Raina, A. K., & Perry, G.
Affiliations
  • Case Western Reserve University (US)
  • Asahikawa Medical College Hospital (JP)
Corresponding author
Smith, Mark A.
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher
Elsevier BV
Published
2000-07
Volume
1502
Issue
1
Pages
139-144
ISSN
0925-4439 (ISSN-L)
OpenAlex
W1983789627
Cited by
895
References
52
Citations by year
2026: 13 · 2025: 22 · 2024: 30 · 2023: 33 · 2022: 31 · 2021: 38 · 2020: 36 · 2019: 40 · 2018: 37 · 2017: 26 · 2016: 33 · 2015: 34 · 2014: 32 · 2013: 39 · 2012: 39
FWCI
5.89
Type
journal article
Language
en
Open access
Locations
  • Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Biochimica et Biophysica Acta
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
oxidative stress, Alzheimer's disease, redox imbalance, free radicals, mitochondrial dysfunction, amyloid-beta, apolipoprotein E, presenilin, amyloid plaques, neurofibrillary tangles, pyramidal neurons, pathogenesis
MeSH terms
Alzheimer Disease, Antioxidants, Free Radicals, Humans, Neurons, Oxidation-Reduction, Peptide Fragments, Amyloid beta-Peptides, Neurofibrillary Tangles, Oxidative Stress, Plaque, Amyloid

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