Human life develops and expands not only in time and space, but also in the retrograde permanent recollection and interweaving of memories. Therefore, individual human identity depends fully on a proper access to the autobiographical memory. Such access is hindered or lost under pathological conditions such as Alzheimer's disease, including recently associated oxidant pathologies, such as ocular neural degeneration occurring in glaucoma or neurosensorial degeneration occurring in Menière's disease. Oxidative stress and altered antioxidant systems have been suggested to play a role in the aetiology of major neurodegenerative disorders, and altered expression of genes sensing oxidative stress, as well as decreased cellular stress response mechanisms could synergistically contribute to the course of these oxidant disorders. Thus, the theory that low levels of stress can produce protective responses against the pathogenic processes is a frontier area of neurobiological research focal to understanding and developing therapeutic approaches to neurodegenerative disorders. Herein, we discuss cellular mechanisms underlying AD neuroinflammatory pathogenesis that are contributory to Alzheimer's disease. We describe endogenous cellular defence mechanism modulation and neurohormesis as a potentially innovative approach to therapeutics for AD and other neurodegenerative conditions that are associated with mitochondrial dysfunction and neuroinflammation. Particularly, we consider the emerging role of the inflammasome as an important component of the neuroprotective network, as well as the importance of Coriolus and Hericium nutritional mushrooms in redox stress responsive mechanisms and neuroprotection.

中文翻译：

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阿尔茨海默氏病和阿尔茨海默氏症相关疾病的发病机理中的神经炎症和神经兴奋：营养蘑菇的调节。

人的生命不仅在时间和空间上发展，而且在逆行中永久地回忆和交织在一起。因此，个人的身份完全取决于对自传式记忆的正确访问。在诸如阿尔茨海默氏病的病理条件下，包括最近相关的氧化剂病理，例如在青光眼中发生的眼神经变性或在梅尼埃病中发生的神经感觉变性，这种进入受到阻碍或丧失。已经表明氧化应激和抗氧化系统的改变在主要神经退行性疾病的病因中起作用，并且感测氧化应激的基因表达的改变以及细胞应激反应机制的降低可以协同促成这些氧化疾病的进程。因此，低压力可以产生针对病原过程的保护性反应的理论是神经生物学研究的前沿领域，致力于理解和发展神经退行性疾病的治疗方法。在这里，我们讨论潜在的AD神经炎性发病机制的细胞机制，这是阿尔茨海默氏病的原因。我们将内源性细胞防御机制的调节和神经兴奋性描述为一种潜在的创新方法，用于治疗AD和其他与线粒体功能障碍和神经炎症相关的神经退行性疾病。特别是，我们认为炎症小体的新兴作用是神经保护网络的重要组成部分，