Filograna Roberta, Beltramini Mariano, Bubacco Luigi, Bisaglia Marco
Molecular Physiology and Biophysics Unit, Department of Biology, University of Padova, Via Ugo Bassi 58B, 35121 Padova, Italy.
Curr Neuropharmacol. 2016;14(3):260-71. doi: 10.2174/1570159x13666151030102718.
Parkinson's disease (PD) is a degenerative neurological syndrome, which is characterized by the preferential death of dopaminergic (DAergic) neurons in the Substantia Nigra. The pathogenesis of this disorder remains poorly understood and PD is still incurable. Current drug treatments are aimed primarily for the treatment of symptoms to improve the quality of life. Therefore, there is a need to find out new therapeutic strategies that not only provide symptomatic relief but also halt or reverse the neuronal damage hampering PD progression. Oxidative stress has been identified as one of the major contributors for the nigral loss in both sporadic and genetic forms of PD. In this review we first evaluate the current literature that links oxidative stress and mitochondrial dysfunction to PD. We then consider the results obtained through the treatment of animal models or PD patients with molecules that prevent oxidative stress or reduce mitochondrial dysfunction.
帕金森病（PD）是一种退行性神经综合征，其特征是黑质中多巴胺能（DAergic）神经元的选择性死亡。这种疾病的发病机制仍知之甚少，且PD仍然无法治愈。目前的药物治疗主要旨在缓解症状以提高生活质量。因此，有必要找到新的治疗策略，不仅能缓解症状，还能阻止或逆转阻碍PD进展的神经元损伤。氧化应激已被确定为散发性和遗传性PD黑质损伤的主要促成因素之一。在本综述中，我们首先评估将氧化应激和线粒体功能障碍与PD联系起来的现有文献。然后，我们考虑通过用预防氧化应激或减少线粒体功能障碍的分子治疗动物模型或PD患者所获得的结果。
