学习记忆障碍给社会及患者带来庞大的精神和经济压力，目前尚无有效的治疗方法，其机制也不清楚。我们前期的系列研究显示，DCF1敲除小鼠与野生型相比，学习记忆能力明显减弱，树突棘密度降低，形成的突触减少，基因芯片分析表明ATP11B在DCF1敲除小鼠中的表达量明显下调。ATP11B定位于神经细胞的突触区，而突触可塑性是构成学习与记忆的神经化学基础。因此，我们提出假设：在DCF1剔除小鼠中，ATP11B表达量下调，在突触发生和传递的过程中，下调的ATP11B抑制细胞膜结构发生改变，影响突触的结构和功能；同时，阻碍突触囊泡的形成和运输，进而影响其下游信号分子的运输及信号通路，削弱了DCF1敲除小鼠的学习记忆能力。本项目拟从分子、细胞和动物水平上并辅以计算生物学手段研究ATP11B对突触的影响及对学习记忆的调控机制，对以突触为基础的学习记忆的研究提供了理论基础，并进一步为学习记忆的治疗开拓了新的思路。

Patients who lost learning and memory function suffered mentally and economically. There is no effective treatment and the mechanism is unclear. Our previous studies show that DCF1-/- mice exhibit weaker learning and memory ability, significant reduction in the spine density within hippocampus, and decreased synapses. Subsequently, gene chip analysis shows that ATP11B is significantly downregulated in DCF1-/- mice. Interestingly, ATP11B is observed localized in the synaptic region of neural cells, and moreover, synaptic plasticity is known to be a cellular mechanism of learning and memory processes. Therefore, we hypothesized that ATP11B is downregulated in DCF1-/- mice, that decreased ATP11B inhibits the membrane structure formation, and that finally affects the structure and function of the synapse. Meanwhile, decreased ATP11B can hinder the formation and trafficking of synaptic vesicles, interfere with the signaling pathway, and subsequently impair the learning and memory ability of DCF1-/- mice. The elucidation of the molecular mechanism underlying synaptic plasticity is important for the understanding of learning and memory ability.Furthermore, it may offer enormous potential for the treatment of a variety of patients who have lost Learning and memory.