Geniposide decreases the level of Aβ1-42 in the hippocampus of streptozotocin-induced diabetic rats.

Although cognitive dysfunction in diabetic patients has been explored extensively, diabetic complications of the central nervous system have not been studied. We have reported previously that geniposide has neurotrophic and neuroprotective activities with the activation of glucagons-like peptide 1 receptor, and regulates glucose-stimulated insulin secretion in vitro. But the role of geniposide on diabetic complications, especially on the neurodegenerative diseases, remains to be investigated. In this study, we investigated the effect of geniposide on the level of Aβ1-42 in the hippocampi of streptozotocin-induced diabetic rats and explored its possible mechanism. The results demonstrated that, accompanied with the improvement of insulin and blood glucose, treatment with geniposide decreased the Aβ1-42 level and improved the expression of insulin-degrading enzyme, which is the key degrading enzyme of Aβ peptide. The results of present study will help to understand the biochemical mechanisms of neuronal dysfunction and death in diabetes and to develop an efficient therapeutic strategy on Alzheimer's disease.