Alavez-Rubio Jessica Sarahi, Juarez-Cedillo Teresa
Universidad Nacional Autónoma de México, Mexico City, Mexico.
Unidad de Investigación Epidemiológica y en Servicios de Salud, Área de Envejecimiento, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.
J Alzheimers Dis Rep. 2024 Jan 12;8(1):43-56. doi: 10.3233/ADR-230112. eCollection 2024.
Dementia is a syndrome in which there is deterioration in memory, behavior, and the ability to perform everyday activities. Alzheimer's disease and vascular dementia are the most common forms of dementia. There is evidence supporting the hypothesis that inflammatory and immune mechanisms are involved in dementia. Microglia, the resident macrophage tissues in the central nervous system, play a significant role in neuroinflammation and play an important role in amyloid-β clearance in the brain, and impaired microglial clearance of amyloid-β has also been shown to be involved in the pathogenesis of Alzheimer's disease. However, there is also abundant evidence that microglia have harmful actions in dementia. Once activated, they can mediate uptake at neuronal synapses. They can also exacerbate tau pathology and secrete deleterious inflammatory factors that can directly or indirectly damage neurons. Thus, depending on the stage of the disease, microglia can act both protectively and detrimentally. Therefore, it is still necessary to continue with studies to better understand the role of microglia in the pathology of dementia. Currently available drugs can only improve cognitive symptoms, have no impact on progression and are not curative, so identifying and studying new therapeutic approaches is important. Considering the role played by microglia in this pathology, it has been pointed out as a possible therapeutic approach. This manuscript aims to address the relationship between microglia and dementia and how this relationship could be used for therapeutic purposes.
痴呆是一种综合征,其特征为记忆、行为以及进行日常活动的能力出现衰退。阿尔茨海默病和血管性痴呆是痴呆最常见的形式。有证据支持炎症和免疫机制参与痴呆的假说。小胶质细胞是中枢神经系统中的常驻巨噬细胞组织,在神经炎症中起重要作用,并且在大脑中β-淀粉样蛋白的清除过程中发挥重要作用,而且小胶质细胞对β-淀粉样蛋白的清除受损也已被证明与阿尔茨海默病的发病机制有关。然而,也有大量证据表明小胶质细胞在痴呆中具有有害作用。一旦被激活,它们可以介导在神经元突触处的摄取。它们还可以加剧tau病理变化并分泌有害的炎症因子,这些因子可直接或间接损害神经元。因此,根据疾病阶段,小胶质细胞既可以起到保护作用,也可以产生有害作用。所以,仍有必要继续开展研究,以更好地了解小胶质细胞在痴呆病理中的作用。目前可用的药物只能改善认知症状,对疾病进展没有影响,也无法治愈,因此确定并研究新的治疗方法很重要。考虑到小胶质细胞在这种病理中的作用,它已被指出是一种可能的治疗方法。本手稿旨在探讨小胶质细胞与痴呆之间的关系,以及这种关系如何用于治疗目的。