Lin Kooi Ong, PhD
This article by Wang and colleagues aimed to investigate the impact of diabetes on brain recovery after stroke using a preclinical model, comparing wild type male mice to diabetes (db/db) mice. The team observed a significant decrease in sensorimotor performance in diabetes mice after stroke. It should be noted that the team did not observe deficit in memory function using the Morris water maze. There was an exacerbated white matter damage at both structural and functional levels. Further, there was an enhanced inflammatory response at the white matter in diabetes mice after stroke, such as a shift of microglia/macrophage to pro-inflammatory phenotype and higher levels of IL-1β and IL-6 expression. The inflammatory environment inhibited oligodendrogenesis, a brain repair mechanism to generate new myelinating oligodendrocytes. These findings provide compelling preclinical evidence that diabetic condition exacerbates functional deficits after stroke.
People with high blood pressure or diabetes are most at risk for stroke. There are several clinical studies documenting that diabetic condition worsens functional outcomes after stroke. There are multiple avenues to consider in terms of advancing the findings in the current study. Firstly, treatment strategies to ameliorate diabetic condition would require further attention, particularly in stroke survivors. Secondly, the pro-inflammatory processes in response to stroke may represent an attractive target to promote white matter repair and functional recovery. Thirdly, replication experiments in different diabetic models using both male and female aged animals are warranted for clinical transaction into the human population.