PPARγplays an important role in improvement of cognitive decline in Alzheimer's disease model animals complicated by lifestyle deseases.

我们制作了阿尔茨海默病模型动物，使其并发脑血管疾病，并证明了迷宫学习障碍等记忆缺陷加重。推测脑血管病所致痴呆的发生可能与海马CA1区TNFα、HMGB1等炎性细胞因子的短暂性升高及神经元凋亡有关。此外，我们能够通过激活具有抗炎作用和抗凋亡作用的PPARγ来改善空间记忆障碍。证明具有PPARγ激动剂作用的药物有望成为痴呆治疗药物。

We made Alzheimer's disease model animals to complicate cerebrovascular disorders, and we proved that defects of memory such as the maze learning disability aggravated. It was supposed that the temporal increase of inflammatory cytokines including TNFα and HMGB1 and apoptosis of neurons in the hippocampus CA1 leaded with the onset of dementia by the cerebrovascular disorders. Furthermore, We were able to improve a spatial memory disorder by activating PPARγwith anti-inflammatory effect and anti-apoptosis effect. It was proved that drugs with PPARγ agonist effect could become the dementia therapeutic drug than this study.