Abstract：
Reactive oxygen species (ROS) are metabolic by-products that constitute an indispensable component of physiological processes, albeit their heightened presence may proffer substantial perils to biological entities. Such a proliferation gives rise to a gradual escalation of oxidative stress within the organism, thereby compromising mitochondrial functionality and inflicting harm upon various bodily systems, with a particular predilection for the central nervous system. In its nascent stages, it is plausible that inflammation has been a facilitator in the progression of the malady. The precise role of inflammation in Alzheimer\'s disease (AD) remains somewhat enigmatic, although it is conceivable that activated microglia and astrocytes might be implicated in the removal of amyloid-β (Aβ) deposits. Nonetheless, prolonged microglial activation is associated with Tau phosphorylation and Aβ aggregation. Research studies have indicated that AD brains upregulate complementary molecules, inflammatory cytokines, acute phase reacting agents, and other inflammatory mediators that may cause neurodegeneration. In this review, oxidative damage products will be discussed as potential peripheral biomarkers for AD and its early stages. The disordered excretion of pro-inflammatory cytokines, chemokines, oxygen, and nitrogen-reactive species, along with the stimulation of the complement system by glial cells, has the potential to disrupt the functionality of neuronal termini. This perturbation, in turn, culminates in compromised synaptic function, a phenomenon empirically linked to the manifestation of cognitive impairments. The management of neurodegenerative conditions in the context of dementia necessitates therapeutic interventions that specifically target the excessive production of inflammatory and oxidative agents. Furthermore, we shall deliberate upon the function of microglia and oxidative injury in the etiology of AD and the ensuing neurodegenerative processes.
摘要：
活性氧（ROS）是代谢副产物，构成生理过程不可或缺的组成部分，尽管它们的存在增加可能会给生物实体带来重大危险。这种增殖导致生物体内氧化应激的逐渐升级，从而损害线粒体功能并对各种身体系统造成伤害，对中枢神经系统有特殊的偏爱。在它的新生阶段，炎症似乎是疾病发展的促进因素。炎症在阿尔茨海默病（AD）中的确切作用仍然有些神秘，尽管可以想象活化的小胶质细胞和星形胶质细胞可能与淀粉样β（Aβ）沉积物的去除有关。尽管如此，延长的小胶质细胞活化与Tau磷酸化和Aβ聚集有关。研究表明，AD大脑上调互补分子，炎性细胞因子，急性期反应剂，和其他可能导致神经变性的炎症介质。在这次审查中,氧化损伤产物将作为AD及其早期的潜在外周生物标志物进行讨论。促炎细胞因子的无序排泄，趋化因子,氧气,和氮反应性物种，随着神经胶质细胞对补体系统的刺激，有可能破坏神经元末端的功能。这种扰动，反过来,最终导致突触功能受损，一种与认知障碍表现有经验联系的现象。在痴呆的背景下神经退行性疾病的管理需要特异性地针对炎性和氧化剂的过度产生的治疗干预。此外，我们将探讨小胶质细胞和氧化损伤在AD的病因和随后的神经退行性过程中的功能。
