Cited by 204Alzheimer's disease research and treatmentsNeurological Disorders and TreatmentsAntioxidant Activity and Oxidative Stress

Oxidative Nerve Cell Death in Alzheimers Disease and Stroke: Antioxidants as Neuroprotective Compounds

Behl, C., Moosmann, B.·2002·Biological Chemistry

Abstract

Many neurodegenerative disorders and syndromes are associated with an excessive generation of reactive oxygen species (ROS) and oxidative stress. The pathways to nerve cell death induced by diverse potential neurotoxins such as peptides, excitatory amino acids, cytokines or synthetic drugs commonly share oxidative downstream processes, which can cause either an acute oxidative destruction or activate secondary events leading to apoptosis. The pathophysiological role of ROS has been intensively studied in in vitro and in vivo models of chronic neurodegenerative diseases such as Alzheimer's disease (AD) and of syndromes associated with rapid nerve cell loss as occuring in stroke. In AD, oxidative neuronal cell dysfunction and cell death caused by protofibrils and aggregates of the AD-associated amyloid beta protein (Abeta) may causally contribute to pathogenesis and progression. ROS and reactive nitrogen species also take part in the complex cascade of events and the detrimental effects occuring during ischemia and reperfusion in stroke. Direct antioxidants such as chain-breaking free radical scavengers can prevent oxidative nerve cell death. Although there is ample experimental evidence demonstrating neuroprotective activities of direct antioxidants in vitro, the clinical evidence for antioxidant compounds to act as protective drugs is relatively scarce. Here, the neuroprotective potential of antioxidant phenolic structures including alpha-tocopherol (vitamin E) and 17beta-estradiol (estrogen) in vitro is summarized. In addition, the antioxidant and cytoprotective activities of lipophilic tyrosine- and tryptophan-containing structures are discussed. Finally, an outlook is given on the neuroprotective potential of aromatic amines and imines, which may comprise novel lead structures for antioxidant drug design.

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Crossref · 10.1515/bc.2002.053

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Authors
Behl, C., & Moosmann, B.
Affiliations
Max Planck Society (DE)
Venue
Biological Chemistry
Published
2002-01-12
Volume
383
Issue
3-4
Pages
521-36
ISSN
1431-6730 (ISSN-L)
OpenAlex
W2033900283
Cited by
203
References
126
Citations by year
2026: 1 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 6 · 2020: 10 · 2019: 6 · 2018: 3 · 2017: 10 · 2016: 6 · 2015: 10 · 2014: 5 · 2013: 13 · 2012: 13
FWCI
1.68
Type
journal article
Language
en
Open access
closed
Locations
  • Biological Chemistry (publishedVersion)
  • PubMed (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
Alzheimer's disease, stroke, reactive oxygen species, oxidative stress, antioxidants, neuroprotection, amyloid-beta, ischemia-reperfusion injury, alpha-tocopherol, vitamin E, estradiol, estrogen, aromatic amines, imines, apoptosis
MeSH terms
Alzheimer Disease, Animals, Antioxidants, Humans, Cell Death, Oxidative Stress, Neurodegenerative Diseases, Stroke

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