神经细丝是细胞轴突中最重要的细胞骨架蛋白，其数量直接与轴突半径大小相关. 但是神经细丝并不是在轴突中静止不动，而是由分子马达承载，沿微管轨道，源源不断地向轴突中输运，称之为“慢性轴突运输”（Slow Axonal Transport)。细丝的轴突运输对轴突形态的形成及神经信号的正常传导，具有非常重要的作用。细丝的轴突运输发生异常会导致各种神经退行性疾病。 .此项研究将从理论上探讨，关于细丝的磷酸化动态地调控细丝运输和轴突形态的机制。我们提出，神经细丝的磷酸化水平，和磷酸化与去磷酸化的动态过程，通过影响细丝间距，细丝相互作用，细丝与马达相互作用，来调控细丝运输，最终影响轴突形态。此项研究将紧密联系实验数据，发展一套非线性的时空耦合偏微分方程，利用计算机模拟和数学解析的手段，解释实验观测的数据，提供一套细丝磷酸化调控细丝运输和轴突形态的理论机制。

Neurofilament(NF) is one of the most abundant cytoskeletal protein in determining axonal caliber. However, neurofilaments are not static but are continuously transported by molecular motors along microtubule tracks into axon, which is named “slow axonal transport”, and characterized by bidirectional, intermittent and stochastic movement. Slow axonal transport of neurofilaments plays an important role in shaping the morphology of axon and functioning in signal conduction. Defects in slow axonal transport could cause many neurodegenerative diseases..This project will focus on the mechanism of how the dynamics of NF phosphorylation regulates slow axonal transport of NF. We propose that, the dynamic balance between phosphorylation and dephosphorylation of NFs modulates NF interspacing, NF interaction, NF transport, all of which contribute to shape axonal morphology. We will develop a set of non-linear partial differential equations and use computational modeling to interprate the experimentally observed data, and eventually provide a mechanism for understanding the function of phosphorylation of NF in regulating slow axonal transport of NFs and axonal morphology.