Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Neuropharmacology. 2010 Sep-Oct;59(4-5):290-4. doi: 10.1016/j.neuropharm.2010.04.005. Epub 2010 Apr 13.
Oxidative stress is at the forefront of Alzheimer disease (AD) research. While its implications in the characteristic neurodegeneration of AD are vast, the most important aspect is that it seems increasingly apparent that oxidative stress is in fact a primary progenitor of the disease, and not merely an epiphenomenon. Moreover, evidence indicates that a long "dormant period" of gradual oxidative damage accumulation precedes and actually leads to the seemingly sudden appearance of clinical and pathological AD symptoms, including amyloid-beta deposition, neurofibrillary tangle formation, metabolic dysfunction, and cognitive decline. These findings provide important insights into the development of potential treatment regimens and even allude to the possibility of a preventative cure. In this review, we elaborate on the dynamic role of oxidative stress in AD and present corresponding treatment strategies that are currently under investigation.
氧化应激是阿尔茨海默病(AD)研究的前沿领域。虽然它在 AD 特征性神经退行性变中的影响是广泛的,但最重要的方面是,氧化应激似乎越来越明显是疾病的主要起源,而不仅仅是一种伴随现象。此外,有证据表明,在临床和病理 AD 症状(包括淀粉样β沉积、神经纤维缠结形成、代谢功能障碍和认知能力下降)看似突然出现之前,存在一个长期的“休眠期”,其中氧化损伤逐渐积累,实际上导致了这些症状的出现。这些发现为潜在治疗方案的开发提供了重要的见解,甚至暗示了预防治疗的可能性。在这篇综述中,我们详细阐述了氧化应激在 AD 中的动态作用,并提出了目前正在研究的相应治疗策略。