Department of Bioprocess Engineering, Institute of Industrial and Environmental Biotechnology, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.
CNS Neurosci Ther. 2024 Jul;30(7):e14856. doi: 10.1111/cns.14856.
Alzheimer's disease (AD), the main cause of dementia, is characterized by synaptic loss and neurodegeneration. Amyloid-β (Aβ) accumulation, hyperphosphorylation of tau protein, and neurofibrillary tangles (NFTs) in the brain are considered to be the initiating factors of AD. However, this hypothesis falls short of explaining many aspects of AD pathogenesis. Recently, there has been mounting evidence that neuroinflammation plays a key role in the pathophysiology of AD and causes neurodegeneration by over-activating microglia and releasing inflammatory mediators.
PubMed, Web of Science, EMBASE, and MEDLINE were used for searching and summarizing all the recent publications related to inflammation and its association with Alzheimer's disease.
Our review shows how inflammatory dysregulation influences AD pathology as well as the roles of microglia in neuroinflammation, the possible microglia-associated therapeutic targets, top neuroinflammatory biomarkers, and anti-inflammatory drugs that combat inflammation.
In conclusion, microglial inflammatory reactions are important factors in AD pathogenesis and need to be discussed in more detail for promising therapeutic strategies.
阿尔茨海默病（AD）是痴呆症的主要病因，其特征是突触丧失和神经退行性变。大脑中β淀粉样蛋白（Aβ）的积累、tau 蛋白的过度磷酸化和神经原纤维缠结（NFTs）被认为是 AD 的起始因素。然而，这一假说并不能解释 AD 发病机制的许多方面。最近有越来越多的证据表明，神经炎症在 AD 的病理生理学中起着关键作用，通过过度激活小胶质细胞和释放炎症介质导致神经退行性变。
使用 PubMed、Web of Science、EMBASE 和 MEDLINE 搜索并总结了所有与炎症及其与阿尔茨海默病的关系相关的最新出版物。
我们的综述展示了炎症失调如何影响 AD 病理学，以及小胶质细胞在神经炎症中的作用、可能的小胶质细胞相关治疗靶点、顶级神经炎症生物标志物和抗炎药物对抗炎症的作用。
总之，小胶质细胞炎症反应是 AD 发病机制中的重要因素，需要更详细地讨论，以寻找有前途的治疗策略。
