Alzheimer´s disease (AD) stands out as the most common chronic neurodegenerative disorder. AD is characterized by progressive cognitive decline and memory loss, with neurodegeneration as its primary pathological feature. The role of neuroinflammation in the disease course has become a focus of intense research. While microglia, the brain’s resident macrophages, have been pivotal to study central immune inflammation, recent evidence underscores the contributions of other cellular entities to the neuroinflammatory process. In this article, we review the inflammatory role of microglia and astrocytes, focusing on their interactions with AD’s core pathologies, amyloid beta deposition, and tau tangle formation. Additionally, we also discuss how different modes of regulated cell death in AD may impact the chronic neuroinflammatory environment. This review aims to highlight the evolving landscape of neuroinflammatory research in AD and underscores the importance of considering multiple cellular contributors when developing new therapeutic strategies.

阿尔茨海默病 (AD) 是最常见的慢性神经退行性疾病。 AD以进行性认知衰退和记忆丧失为特征，以神经变性为其主要病理特征。神经炎症在疾病过程中的作用已成为深入研究的焦点。虽然小胶质细胞（大脑中的常驻巨噬细胞）对于研究中枢免疫炎症至关重要，但最近的证据强调了其他细胞实体对神经炎症过程的贡献。在本文中，我们回顾了小胶质细胞和星形胶质细胞的炎症作用，重点关注它们与 AD 核心病理、β 淀粉样蛋白沉积和 tau 缠结形成的相互作用。此外，我们还讨论了 AD 中不同的调节细胞死亡模式如何影响慢性神经炎症环境。本综述旨在强调 AD 神经炎症研究的不断发展，并强调在制定新的治疗策略时考虑多种细胞因素的重要性。