Alzheimer's disease (AD) is one of the most prevailing neurodegenerative disorders of elderly humans associated with cognitive damage. Biochemical, epigenetic, and pathophysiological factors all consider a critical role of extracellular amyloid-beta (Aß) plaques and intracellular neurofibrillary tangles (NFTs) as pathological hallmarks of AD. In an endeavor to describe the intricacy and multifaceted nature of AD, several hypotheses based on the roles of Aß accumulation, tau hyperphosphorylation, impaired cholinergic signaling, neuroinflammation, and autophagy during the initiation and advancement of the disease have been suggested. However, in no way do these theories have the potential of autonomously describing the pathophysiological alterations located in AD. The complex pathological nature of AD has hindered the recognition and authentication of successful biomarkers for the progression of its diagnosis and therapeutic strategies. There has been a significant research effort to design multi-target-directed ligands for the treatment of AD, an approach which is developed by the knowledge that AD is a composite and multifaceted disease linked with several separate but integrated molecular pathways.

阿尔茨海默病 (AD) 是与认知损伤相关的老年人最普遍的神经退行性疾病之一。生化、表观遗传和病理生理因素都认为细胞外淀粉样蛋白-β (Aß) 斑块和细胞内神经原纤维缠结 (NFT) 是 AD 的病理标志。为了描述 AD 的复杂性和多面性，已经提出了几个假设，这些假设基于 Aß 积累、tau 过度磷酸化、胆碱能信号传导受损、神经炎症和自噬在疾病的开始和发展过程中的作用。然而，这些理论绝不可能自主描述 AD 中的病理生理学改变。AD 的复杂病理性质阻碍了对其诊断和治疗策略进展的成功生物标志物的识别和鉴定。已经进行了重大的研究工作来设计用于治疗 AD 的多靶点定向配体，这种方法是基于 AD 是一种复合和多方面疾病的知识而开发的，它与几个独立但整合的分子途径相关联。