Next, we found that calcitonin treatment could shorten the escape latency, increase the frequency of entering the target quadrant and time of staying in the platform quadrant, and reduce the total movement distance in the mice with CKD; whereas, overexpression of Drp1 significantly counteracted the promotive effect of calcitonin on learning and memory functions in CKD mice (Fig. 3D). This evidence concerns the gene DNM1L and chronic kidney disease.