[关键词]
[摘要]
由于人口老年化的进展,阿尔茨海默病(Alzheimer’s disease,AD)的发病率呈上升趋势,认知障碍是其主要症状,但其发病机制尚不明确。最新的研究证实,AD的发病与代谢紊乱及免疫应激有密切联系,是一种涉及“代谢-免疫-中枢神经系统”网络的全身系统性疾病。骨髓来源的先天免疫细胞巨噬细胞处于代谢-免疫-中枢神经系统的交叉点。藏医“整体观”对于全身系统性疾病的多靶点调控治疗更具优势。藏医理论中,黄水病的产生与饮食摄入及代谢紊乱关系密切,这与现代医学中糖尿病-免疫系统疾病相关联的发病机制吻合,因此黄水病经典治疗方在AD所致的认知障碍治疗中有潜在的应用价值。通过对AD“代谢-免疫-中枢神经系统”发病机制、藏医中黄水病理论的关系,及经典黄水病治疗方在临床实践及实验研究中对认知障碍、神经系统保护方面的疗效及机制研究进行综述,为该类药物防治认知障碍的特色作用机制阐释与新药二次开发提供理论参考与科学依据。
[Key word]
[Abstract]
The prevalence of Alzheimer's disease (AD) is increasing as the population ages, with cognitive dysfunction being the primary symptom, but the pathogenesis remains uncertain. Recent research has demonstrated that the beginning of AD is closely related to metabolic irregularities and immunological stress, and that it is a systemic disease involving the "metabolism-immune-central nervous system" network. Macrophages, which are generated in bone marrow, are at the crosslink of metabolism, immunity, and the central nervous system. The “holistic view” of Tibetan medicine is preferable for multi-target management and systemic illness treatment. According to Tibetan medicine theory, “Huang-Shui” disease is a strong connection with nutrition consumption and digestion disorders, which is similar with the pathophysiology of diabetes associated with immune system diseases in modern medicine. Therefore, the traditional therapy of “Huang-Shui” disease has potential applicability in the treatment of AD cognitive disorder. This paper reviewed the AD’s pathogenesis involving “metabolism-immune-central nervous system” and its relationship to Tibetan medicine’s theory of “Huang-Shui” disease, as well as efficacy and mechanism studies of classical “Huang-Shui” prescriptions on cognitive impairment and nervous system protection in clinical practices and experiments, to provide a theoretical reference and scientific basis for future development.
[中图分类号]
R285
[基金项目]
国家自然科学基金资助项目(82174083);四川省科技厅青年科学基金项目(2022NSFSC1437);四川省中医药管理局科学技术研究专项课题(2021MS121);西南民族大学中央高校基本科研业务费专项资金项目(ZYN2022040);西南民族大学青藏高原研究科技创新团队项目(2024CXTD16)