The Src family non-receptor tyrosine kinase Fyn has been implicated in neurodegeneration of Alzheimer’s disease through interaction with amyloid β (Aβ). However, the role of Fyn in the pathogenesis of primary tauopathies such as FTDP-17, where Aβ plaques are absent, is poorly understood. In the current study, we used AAV2/8 vectors to deliver tauP301L to the brains of WT and Fyn KO mice, generating somatic transgenic tauopathy models with the presence or absence of Fyn. Although both genotypes developed tau pathology, Fyn KO developed fewer neurofibrillary tangles on Bielschowsky and Thioflavin S stained sections and showed lower levels of phosphorylated tau. In addition, tauP301L-induced behavior abnormalities and depletion of synaptic proteins were not observed in the Fyn KO model. Our work provides evidence for Fyn being a critical protein in the disease pathogenesis of FTDP-17.

中文翻译：

---

Fyn 消耗改善了 tauP301L 诱导的神经病理学。

Src 家族非受体酪氨酸激酶 Fyn 通过与淀粉样蛋白 β (Aβ) 的相互作用与阿尔茨海默病的神经变性有关。然而，人们对 Fyn 在原发性 tauopathies（如 FTDP-17，其中不存在 Aβ 斑块）的发病机制中的作用知之甚少。在当前的研究中，我们使用 AAV2/8 载体将 tauP301L 递送到 WT 和 Fyn KO 小鼠的大脑，生成具有或不存在 Fyn 的体细胞转基因 tau 蛋白病模型。尽管这两种基因型都发生了 tau 病理，但 Fyn KO 在 Bielschowsky 和硫磺素 S 染色切片上发生的神经原纤维缠结较少，并且磷酸化 tau 水平较低。此外，在 Fyn KO 模型中未观察到 tauP301L 诱导的行为异常和突触蛋白消耗。