The pathogenesis of Alzheimer’s disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain’s vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer’s disease. OS and Aβ are linked to each other because Aβ induces OS, and OS increases the Aβ deposition. Thus, the answer to the question “which comes first: the chicken or the egg?” remains extremely difficult. In any case, the evidence for the primary occurrence of oxidative stress in AD is attractive. Thus, evidence indicates that a long period of gradual oxidative damage accumulation precedes and results in the appearance of clinical and pathological AD symptoms, including Aβ deposition, neurofibrillary tangle formation, metabolic dysfunction, and cognitive decline. Moreover, oxidative stress plays a crucial role in the pathogenesis of many risk factors for AD. Alzheimer’s disease begins many years before its symptoms, and antioxidant treatment can be an important therapeutic target for attacking the disease.

中文翻译：

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阿尔茨海默病中的氧化应激和β淀粉样蛋白。先有鸡还是先有蛋？

阿尔茨海默病的发病机制涉及已知可诱导突触功能障碍和神经变性的 β 淀粉样蛋白 (Aβ) 积累。大脑对氧化应激 (OS) 的脆弱性被认为是阿尔茨海默病的关键不利因素。OS 和 Aβ 相互关联，因为 Aβ 诱导 OS，而 OS 增加 Aβ 沉积。因此，问题的答案是“先有鸡还是先有蛋？” 仍然非常困难。无论如何，AD 中氧化应激主要发生的证据是有吸引力的。因此，有证据表明，长时间的逐渐氧化损伤积累先于并导致临床和病理性 AD 症状的出现，包括 Aβ 沉积、神经原纤维缠结形成、代谢功能障碍和认知能力下降。而且，氧化应激在 AD 的许多危险因素的发病机制中起着至关重要的作用。阿尔茨海默病在其症状出现之前很多年就开始了，抗氧化治疗可以成为攻击这种疾病的重要治疗目标。