The Effect of Endurance Training on the Expression of PRDX6 and KAT2B Genes in Hippocampus of Beta Amyloid-Induced Rat Model of Alzheimer's Disease: An Experimental Study

Alzheimer's disease is the most common form of dementia. KAT2B (Lysine Acetyltransferase 2B) is a mitochondrial protein known as mitochondria clearing control organ by mitophagy. PRDX6 (Peroxiredoxin 6) is a key regulator of mitophagy and plays a critical role in maintaining mitochondrial ROS (Reactive oxygen species) homeostasis. Therefore, the purpose of this study was to investigate the effect of swimming endurance training on expression of PRDX6 and KAT2B genes in male hippocampus model of Wistar rat after induction of Alzheimer's.

In this experimental study, 18 rats were randomly divided into 3 groups including control, Alzheimer's and exercise-Alzheimer's groups. The Alzheimer's model was created by injecting beta 42-1 amyloid into the CA1 hippocampus region, and the training group rats participated in the swimming 30 min/day for a period of 3 weeks. In order to confirm the Alzheimer's model, thioflavin staining was used, and Real Time PCR method was used to determine the expression of the desired genes. One-way ANOVA with Tukey’s post-hoc test was used for data analysis.

There was a significant difference between the amount of beta-amyloid plaques in the two groups of Alzheimer's and control (p<0.001). Alzheimer's disease significantly reduced the expression of PRDX6 and KAT2B genes in the Alzheimer's rats hippocampus (p<0.001), and also following the endurance exercise, the PRDX6 gene expression increased compared with the Alzheimer's group (p=0.027).

Endurance training can possibly maintain oxidative balance and improve mitochondrial hemostasis in Alzheimer's disease.