Mechanism of Autonomic Exercise Improving Cognitive Function of Alzheimer's Disease by Regulating lncRNA SNHG14

This paper studied the influence of exercise on the cognitive ability of AD patients and elucidated potential mechanisms. The expression of SNHG14 was validated by qRT-PCR. The cognitive impairment of mice was examined by MWM Test. ELISA tests were applied to discover the influence of SNHG14 on inflammation. Overexpression of SNHG14 was found in AD patients and underexpression of SNHG14 was identified in these AD patients after exercise. In APP/PS1 double transgenic mice, SNHG14 reversed the protective impacts of exercise on escape latency and distance moved. The upregulation of SNHG14 also inhibited the effects of exercise on the percentage of time spent in the target quadrant and times of platform crossing. Besides, overexpression of SNHG14 reversed the repressed expression of IL-6, IL-1 beta, and TNF-alpha. In total, exercise could ameliorate cognitive disorder and inflammation activity by reducing the levels of SNHG14.

Automated summary

Exercise was found to reduce the levels of SNHG14, which in turn ameliorated cognitive disorder and inflammation activity in AD patients. In mouse experiments, SNHG14 reversed the protective impacts of exercise on cognitive ability and inflammation.