Antioxidant neuroprotection in Alzheimer’s disease as preventive and therapeutic approach2 2This article is part of a series of reviews on “Causes and Consequences of Oxidative Stress in Alzheimer’s Disease.” The full list of papers may be found on the homepage of the journal.
2002; Elsevier BV; Volume: 33; Issue: 2 Linguagem: Inglês
10.1016/s0891-5849(02)00883-3
ISSN1873-4596
AutoresChristian Behl, Bernd Moosmann,
Tópico(s)Free Radicals and Antioxidants
ResumoVarious neurodegenerative disorders and syndromes are associated with oxidative stress. The deleterious consequences of excessive oxidations and the pathophysiological role of reactive oxygen species (ROS) have been intensively studied in Alzheimer's disease (AD). Neuronal cell dysfunction and oxidative cell death caused by the AD-associated amyloid β protein may causally contribute to the pathogenesis of AD. Antioxidants that prevent the detrimental consequences of ROS are consequently considered to be a promising approach to neuroprotection. While there is ample experimental evidence demonstrating neuroprotective activities of antioxidants in vitro, the clinical evidence that antioxidant compounds act as protective drugs is still relatively scarce. Nevertheless, antioxidants constitute a major part of the panel of clinical and experimental drugs that are currently considered for AD prevention and therapy. Here, focus is put mainly on phenolic antioxidant structures that belong to the class of direct antioxidants. Experimental and clinical evidence for the neuroprotective potential of α-tocopherol (vitamin E) and 17β-estradiol (estrogen) is shortly summarized and an outlook is given on possible novel antioxidant lead structures with improved pharmacological features.
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