Alzheimer's disease: from molecular pathways to therapies

阿尔茨海默病:从分子通路到治疗

阅读:4

Abstract

Alzheimer disease (AD) is the most common neurodegenerative disorder and a leading cause of dementia worldwide. With accelerating population aging, its incidence continues to rise, imposing a substantial burden on public health systems and society. Despite extensive advances in research, currently available therapies remain largely symptomatic and have limited capacity to halt or reverse disease progression. Recent progress in understanding the molecular and cellular mechanisms underlying AD has driven the development of targeted therapeutic strategies, particularly immunotherapies directed against amyloid-β (Aβ) and tau pathology. However, the pathogenesis of AD is highly complex and multifactorial, underscoring the need for a more integrated understanding of the interactions among diverse pathological processes and the identification of additional therapeutic targets. Here, we provide a systematic synthesis of the core pathological mechanisms of AD and their interconnected molecular pathways, together with a comprehensive overview of current targeted therapeutic strategies. We highlight recent advances in Aβ- and tau-directed immunotherapies and further examine emerging interventions targeting neuroinflammation, metabolic dysregulation, the gut microbiota, lifestyle-related factors, and neurogenesis, evaluating their potential based on evidence from both clinical and preclinical studies. By integrating mechanistic insights with therapeutic developments, this review outlines key opportunities and challenges in the evolving landscape of AD treatment. These perspectives may inform the development of next-generation disease-modifying therapies and contribute to a more comprehensive framework for understanding the pathogenesis and treatment of AD.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。