Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA;
Pharmaceuticals (Basel). 2012;5(10):1103-19. doi: 10.3390/ph5101103.
In neuronal systems, the health and activity of mitochondria and synapses are tightly coupled. For this reason, it has been postulated that mitochondrial abnormalities may, at least in part, drive neurodegeneration in conditions such as Alzheimer's disease (AD). Mounting evidence from multiple Alzheimer's disease cell and mouse models and postmortem brains suggest that loss of mitochondrial integrity may be a key factor that mediates synaptic loss. Therefore, the prevention or rescue of mitochondrial dysfunction may help delay or altogether prevent AD-associated neurodegeneration. Since mitochondrial health is heavily dependent on antioxidant defenses, researchers have begun to explore the use of mitochondria-targeted antioxidants as therapeutic tools to prevent neurodegenerative diseases. This review will highlight advances made using a model mitochondria-targeted antioxidant peptide, SS31, as a potential treatment for AD.
在神经元系统中,线粒体和突触的健康和活性紧密相关。因此,有人提出线粒体异常可能至少部分导致阿尔茨海默病(AD)等疾病的神经退行性变。来自多个 AD 细胞和小鼠模型以及尸检大脑的越来越多的证据表明,线粒体完整性的丧失可能是介导突触丧失的关键因素。因此,预防或挽救线粒体功能障碍可能有助于延缓或完全预防 AD 相关的神经退行性变。由于线粒体健康严重依赖于抗氧化防御,研究人员已开始探索使用靶向线粒体的抗氧化剂作为治疗工具来预防神经退行性疾病。本综述将重点介绍使用模型靶向线粒体的抗氧化肽 SS31 作为 AD 潜在治疗方法所取得的进展。