Phosphorylated tau (P-tau) has received much attention in the field of Alzheimer's disease (AD), as a potential therapeutic target owing to its involvement with synaptic damage and neuronal dysfunction. The continuous failure of amyloid β (Aβ)-targeted therapeutics highlights the urgency to consider alternative therapeutic strategies for AD. The present review describes the latest developments in tau biology and function. It also explains abnormal interactions between P-tau with Aβ and the mitochondrial fission protein Drp1, leading to excessive mitochondrial fragmentation and synaptic damage in AD neurons. This article also addresses 3D pharmacophore-based drug models designed to treat patients with AD and other tauopathies.

中文翻译：

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基于药理模型的抗阿尔茨海默氏病磷酸化tau的治疗药物模型。

磷酸化的tau（P-tau）由于其涉及突触损伤和神经元功能障碍，已成为阿尔茨海默氏病（AD）领域的潜在治疗靶标。靶向淀粉样蛋白（Aβ）的治疗药物持续失败，凸显了考虑替代性AD治疗策略的紧迫性。本综述描述了tau生物学和功能的最新发展。它还解释了P-tau与Aβ和线粒体裂变蛋白Drp1之间的异常相互作用，导致AD神经元中的线粒体过度断裂和突触损伤。本文还介绍了基于3D药效团的药物模型，这些药物模型旨在治疗患有AD和其他疾病的患者。