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Oxidative nerve cell death in Alzheimer's disease and stroke: antioxidants as neuroprotective compounds.
Biol Chem. 2002 Mar-Apr; 383(3-4):521-36.BC

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.

Authors+Show Affiliations

Max-Planck-Institute of Psychiatry, Munich, Germany.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

12033440

Citation

Behl, Christian, and Bernd Moosmann. "Oxidative Nerve Cell Death in Alzheimer's Disease and Stroke: Antioxidants as Neuroprotective Compounds." Biological Chemistry, vol. 383, no. 3-4, 2002, pp. 521-36.
Behl C, Moosmann B. Oxidative nerve cell death in Alzheimer's disease and stroke: antioxidants as neuroprotective compounds. Biol Chem. 2002;383(3-4):521-36.
Behl, C., & Moosmann, B. (2002). Oxidative nerve cell death in Alzheimer's disease and stroke: antioxidants as neuroprotective compounds. Biological Chemistry, 383(3-4), 521-36.
Behl C, Moosmann B. Oxidative Nerve Cell Death in Alzheimer's Disease and Stroke: Antioxidants as Neuroprotective Compounds. Biol Chem. 2002 Mar-Apr;383(3-4):521-36. PubMed PMID: 12033440.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative nerve cell death in Alzheimer's disease and stroke: antioxidants as neuroprotective compounds. AU - Behl,Christian, AU - Moosmann,Bernd, PY - 2002/5/30/pubmed PY - 2002/11/26/medline PY - 2002/5/30/entrez SP - 521 EP - 36 JF - Biological chemistry JO - Biol Chem VL - 383 IS - 3-4 N2 - 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. SN - 1431-6730 UR - https://www.unboundmedicine.com/medline/citation/12033440/Oxidative_nerve_cell_death_in_Alzheimer's_disease_and_stroke:_antioxidants_as_neuroprotective_compounds_ L2 - https://www.degruyter.com/document/doi/10.1515/BC.2002.053 DB - PRIME DP - Unbound Medicine ER -