PRG-1作为一种神经元可塑性的调节器，其低表达在糖尿病及神经功能障碍的发病过程中起了重要作用，但低表达的机制仍存许多疑问。我们前期研究发现：糖尿病大鼠海马内PRG-1 基因及蛋白表达均下调、LncRNA NONRATG022419表达下调、miR-18a表达升高，而且NONRATG022419与miR-18a，miR-18a与Prg-1，存在靶向关系。因此提出：在糖尿病状态下， 由于海马内NONRATG022419表达下调，作为ceRNA吸附miR-18a的数量减少，使得miR-18a相对多的结合到靶基因Prg-1上，抑制了蛋白PRG-1的表达，进而影响突触的可塑性，促进了糖尿病脑损伤。本课题拟在2型糖尿病动物模型及神经元细胞模型上，探讨高糖引起NONRATG022419表达降低与PRG-1低表达的关系及这种变化与神经细胞损伤的关联，为糖尿病脑病的治疗提供新的思路。

PRG –1 is as a regulator of neuronal plasticity, which is down-regulated both in diabetes and neurological disorders pathogenesis and that acts an important function, but the mechanism of its down-regulation is still not clearly elucidated.   In our previous studies, both of the PRG –1 gene and protein are detected down-regulated ，LncRNA NONRATG022419 also is down-regulated, and   miR -18a is higher expression in the hippocampus of diabetic rats brain. Moreover,NONRATG022419   can be combined with miR-18a, and miR-18a can be combined with Prg-1. There is a targeted relationship. Therefore, it is postulated that due to the NONRATG022419 downexpression in hippocampus, the number of mir-18a   being adsorbed by NONRATG022419 as   ceRNA   are reduces, which makes miR -18a to relatively more combined with the target genes Prg-1, that inhibits the expression of protein   PRG-1, affects   synaptic plasticity, and   promotes the diabetes brain damage. In this project， we demonstrate the relationship of NONRATG022419 and the   down regulationin of PRG- 1 as well as the neuron damage associated, which would provide a novel idea for the treatment of diabetic encephalopathy.