Casetta I, Govoni V, Granieri E
Istituto di Clinica Neurologica, Dipartimento di Discipline Medico-Chirurgiche della Comunicazione e del Comportamento, Università di Ferrara, Corso della Giovecca 203, I-44100 Ferrara, Italy.
Curr Pharm Des. 2005;11(16):2033-52. doi: 10.2174/1381612054065729.
It is widely accepted that oxidative stress increases with age, and that age is a major risk factor for several neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. An inbalanced overproduction of reactive oxygen species can induce neuronal damage, leading to neuronal death by necrosis or apoptosis. Antioxidants are consequently considered to be a promising approaches to neuroprotection. Although experimental data are consistent in demonstrating a neuroprotective effects of antioxidants in vitro and in animal models, the clinical evidence that antioxidants agents may prevent or slow the course of these diseases is still relatively unsatisfactory, and unsufficient to strongly modify the clinical practice. This review summarizes the available data from experimental studies and clinical trials on antioxidant neuroprotection in Parkinson's and Alzheimer's disease.
人们普遍认为,氧化应激会随着年龄的增长而增加,并且年龄是帕金森病和阿尔茨海默病等几种神经退行性疾病的主要风险因素。活性氧的产生失衡会导致神经元损伤,进而通过坏死或凋亡导致神经元死亡。因此,抗氧化剂被认为是一种有前景的神经保护方法。尽管实验数据一致表明抗氧化剂在体外和动物模型中具有神经保护作用,但抗氧化剂可能预防或减缓这些疾病进程的临床证据仍然相对不足,不足以有力地改变临床实践。这篇综述总结了帕金森病和阿尔茨海默病中抗氧化剂神经保护的实验研究和临床试验的现有数据。