Mechanisms and Intervention Strategies of Beta-Amyloid and Tau Proteins in Alzheimer's Disease
TL;DR
The synergistic pathological network between Aβ and tau is clarified, updated progress on targeted therapies are summarized, and theoretical support for accurate early diagnosis and individualized clinical treatment of AD is offered.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that poses a major threat to the health and quality of life of the aging population worldwide, with its complex and multifactorial pathological mechanisms remaining incompletely elucidated. Mounting evidence indicates that amyloid-beta (Aβ) deposition and tau hyperphosphorylation are not independent events but interact synergistically to drive the onset and progression of AD, creating a self-amplifying pathological cascade. This paper firstly systematically summarizes the biological properties of Aβ and tau proteins, and further explores their synergistic interaction modes and pathogenic effects in the AD pathological cascade. Furthermore, it reviews the latest advances and clinical challenges in targeted therapeutic strategies against Aβ and tau, including antibody-based therapies, small-molecule inhibitors, and gene-targeted interventions. The purpose of this study is to clarify the synergistic pathological network between Aβ and tau, summarize updated progress on targeted therapies, and offer theoretical support for accurate early diagnosis and individualized clinical treatment of AD.