Aliev Gjumrakch, Smith Mark A, Seyidov Dilara, Neal Maxwell Lewis, Lamb Bruce T, Nunomura Akihiko, Gasimov Eldar K, Vinters Harry V, Perry George, LaManna Joseph C, Friedland Robert P
Electron Microscopy Center, and Department of Anatomy, Case Western Reserve University, School of Medicine and University Hospital of the Cleveland, OH 44106-4938, USA.
Brain Pathol. 2002 Jan;12(1):21-35. doi: 10.1111/j.1750-3639.2002.tb00419.x.
Alzheimer's disease (AD) and stroke are two leading causes of age-associated dementia. A rapidly growing body of evidence indicates that increased oxidative stress from reactive oxygen radicals is associated with the aging process and age-related degenerative disorders such as atherosclerosis, ischemia/reperfusion, arthritis, stroke, and neurodegenerative diseases. New evidence has also indicated that vascular lesions are a key factor in the development of AD. This idea is based on a positive correlation between AD and cardiovascular and cerebrovascular diseases such as arterio- and atherosclerosis and ischemia/reperfusion injury. In this review we consider recent evidence supporting the existence of an intimate relationship between oxidative stress and vascular lesions in the pathobiology of AD. We also consider the opportunities for therapeutic interventions based on the molecular pathways involved with these causal relationships.
阿尔茨海默病（AD）和中风是与年龄相关的痴呆症的两大主要病因。越来越多的证据表明，活性氧自由基产生的氧化应激增加与衰老过程以及与年龄相关的退行性疾病有关，如动脉粥样硬化、缺血/再灌注、关节炎、中风和神经退行性疾病。新证据还表明，血管病变是AD发展的关键因素。这一观点基于AD与心血管和脑血管疾病（如动脉硬化和动脉粥样硬化以及缺血/再灌注损伤）之间的正相关关系。在这篇综述中，我们探讨了支持氧化应激与AD病理生物学中的血管病变之间存在密切关系的最新证据。我们还基于与这些因果关系相关的分子途径，考虑了治疗干预的机会。
