Neuroinflammation and microglial dysfunction are key contributors to the development of Alzheimer's disease (AD). Toll-like receptors (TLRs) are transmembrane proteins primarily involved in immune responses and expressed by several immune and non-immune cells within the central nervous system. Signaling of TLRs affects the core of AD changes, including synaptic plasticity, microglial activity, tau phosphorylation, and inflammatory responses. We reviewed the activity, expression, potential applications, and genetic polymorphisms of TLRs in AD. Activation of TLRs has shown both destructive and protective effects. Several genetic polymorphisms of TLRs have been also recognized as protective or risk factors for AD. We concluded that TLRs are one of the major components of AD pathogenesis, particularly in the early stages of the disease, which can provide novel therapeutic options.

中文翻译：

---

阿尔茨海默病中的 Toll 样受体

神经炎症和小胶质细胞功能障碍是阿尔茨海默病 (AD) 发展的关键因素。Toll 样受体 (TLR) 是主要参与免疫反应的跨膜蛋白，由中枢神经系统内的几种免疫和非免疫细胞表达。TLR 信号传导影响 AD 变化的核心，包括突触可塑性、小胶质细胞活性、tau 磷酸化和炎症反应。我们回顾了 AD 中 TLRs 的活性、表达、潜在应用和遗传多态性。TLR 的激活已显示出破坏性和保护性作用。TLR 的几种遗传多态性也被认为是 AD 的保护或危险因素。我们得出结论，TLRs 是 AD 发病机制的主要组成部分之一，尤其是在疾病的早期阶段，