Using the MWM test, the beneficial effect of the senolytic was more obvious in middle-aged male mice, when the treatment was started once the cognitive defects were established: treatment from 9 to 12-mo clearly accelerated the learning process, significantly increased short and delayed memory retention, and tended to decrease p21 and SASP expression in males while having opposite effects on cognition and p21/SASP factors in females. The gene discussed is CDKN1A; the disease is Cognitive impairment.