Growing body of evidence suggests that mitochondrial dysfunctions and resultant oxidative stress are likely responsible for many neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). Aldehyde dehydrogenase (ALDH) superfamily plays a crucial role in several biological processes including development and detoxification pathways in the organism. In particular, ALDH2 is crucial in the oxidative metabolism of toxic aldehydes in the brain, such as catecholaminergic metabolites (DOPAL and DOPEGAL) and the principal product of lipid peroxidation process 4-HNE. This review aims to deepen the current knowledge regarding to ALDH2 function and its relation with brain-damaging processes that increase the risk to develop neurodegenerative disorders. We focused on relevant literature of what is currently known at molecular and cellular levels in experimental models of these pathologies. The understanding of ALDH2 contributions could be a potential target in new therapeutic approaches for PD and AD due to its crucial role in mitochondrial normal function maintenance that protects against neurotoxicity.

越来越多的证据表明，线粒体功能障碍和由此产生的氧化应激可能与许多神经退行性疾病有关，包括阿尔茨海默氏病（AD）和帕金森氏病（PD）。乙醛脱氢酶（ALDH）超家族在生物过程中的几个生物过程（包括发育和解毒途径）中起着至关重要的作用。特别是，ALDH2在大脑中有毒醛（例如儿茶酚胺能代谢产物（DOPAL和DOPEGAL）和脂质过氧化过程4-HNE的主要产物）的氧化代谢中至关重要。这篇综述旨在加深关于ALDH2功能及其与脑损伤过程的关系的当前知识，这种损伤增加了发生神经退行性疾病的风险。我们集中于这些病理学实验模型中分子和细胞水平上目前已知的相关文献。由于ALDH2在保护线粒体正常功能中起着保护神经毒性的关键作用，因此对于PD和AD的新治疗方法的了解可能成为潜在的目标。