医学
疾病
重症监护医学
临床试验
生物标志物
透视图(图形)
临床终点
临床实习
动作(物理)
选择(遗传算法)
神经退行性变
生物信息学
梅德林
医学物理学
淀粉样蛋白(真菌学)
病理
精密医学
终点测定
淀粉样β
治疗方法
生物标志物发现
临床疾病
单克隆抗体
作者
Jie Wu,Chaofan Geng,Liyang Liu,Yi Tang
标识
DOI:10.1016/j.medp.2025.100112
摘要
Alzheimer’s disease (AD) imposes a substantial clinical and societal burden, yet currently approved symptomatic therapies do not modify the underlying disease biology. Recently, three anti-amyloid monoclonal antibodies (aducanumab, lecanemab, and donanemab) have demonstrated robust amyloid clearance. Their clinical effects are statistically significant but modest, underscoring the need for broader, biologically informed strategies. Guided by the 2024 Alzheimer’s Association ATNIVS biomarker framework, this review synthesizes disease-modifying therapies (DMTs) targeting amyloid (A), tau (T), neurodegeneration (N), inflammation (I), vascular injury (V), and α-synuclein (S). For each domain, we summarize mechanisms of action and pivotal clinical trial results, highlighting safety considerations such as amyloid-related imaging abnormalities (ARIA) with anti-amyloid antibodies. We further outline future directions, including biomarker-based staging for trial enrollment, rational combination regimens (for example, anti-amyloid plus anti-tau), and endpoint selection aligned with minimal clinically important differences (MCID). Applying the ATNIVS framework to AD DMT development may accelerate the implementation of mechanism‑matched interventions. This approach can also facilitate precision therapeutics across diverse patient subgroups.
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