摘要
阿尔茨海默氏病(AD)是一种慢性无法治愈的慢性疾病,可导致神经系统恶化,表现为记忆力减退和执行大脑功能受损,影响身体能力,例如智力,患者的常识。阿尔茨海默氏病的最新治疗方法只是症状缓解,进一步显示了针对治疗可怕病理的潜在沉默杀伤进展的治疗策略的需求。因此,当前的研究方向集中在鉴定导致对阿尔茨海默氏病的神经病理学理解的进化的分子机制。当前靶标(淀粉样蛋白β,τ蛋白,氧化应激等)区域中的饱和状态已导致科学界重新思考机械神经退行性途径并重新规划了当前的研究方向。尽管压力的作用已被认识很多年并促进了认知障碍的发展,但压力的领域最近已获得了急需的推动力,并被公认为可改善AD的威胁。压力是人类无法避免的经历,可以解决并正常化,但压力通路的长期激活会破坏生理状态。慢性应激介导的神经内分泌刺激的激活通常与发展AD的高风险有关。慢性应激驱动的生理失调和高皮质醇血症在神经元水平混杂在一起,并导致脑结构的功能性(代谢代谢,兴奋性毒性,炎症)和解剖结构重塑(老年斑,τ缠结,海马萎缩,脊椎退缩),最终导致严重的认知能力下降。本综述旨在收集最相关的证据,这些证据支持慢性应激作为AD的现实且可修改的治疗专用标记,并倡导糖皮质激素受体作为治疗干预措施。
关键词: 压力,糖皮质激素,HPA轴,阿尔茨海默氏病,炎症,β淀粉样蛋白,神经变性。
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