Analysis Of The Characteristics And Mechanism Of Cognitive Impairment Caused By Rapid Eye Movement Sleep Disorder

Objective:To examine the cognitive dysfunction pattern of rapid eye movement sleep behavior disorder.Methods:A total of 116 people were recruited,including 51 rapid eye movement sleep behavior disorder(RBD)diagnosed by polysomnography(24 idiopathic RBD and 27 RBD with parkinson’s disease),35 other sleep disorders(18 obstructive sleep apnea syndrome and 17 others)and 30 healthy controls,from 2015 to 2020 in Shanghai Ruijin hospital.Demographic features were collected and different scales were used to evaluate sleep,cognitive and autonomic function.Results:RBD performed worst in Trail Making Test-B tests among three groups.RBD patients also demonstrated impairments in autonomic function and anxiety mood.In subgroup analysis,idiopathic RBD showed worse performance in Auditory Verbal Learning Test than obstructive sleep apnea.Conclusion:RBD showed executive dysfunction and autonomic dysfunction.Objective:Our study aimed toinvestigatethe changes of Aβ and behavioral function inAPP/PS1 transgenic mice after chronic rapid eye movement sleep deprivation.Methods:A mouse model of Alzheimer’s disease(APP/PS1 transgenic mouse)that can simultaneously express the fusion of human elderin(DeltaE9)and human mouse amyloid precursor protein(APPswe)was used as an animal model.APP/PS1 transgenic mice were divided into two groups:big platform sleep(Only changed the sleep environment but not deprived of sleep)and small platform sleep(deprived of the rapid eye movement sleep).We used the water maze,Y maze experiment and passive avoidance text to detect the behavioral change of the mice.Then we took the plasma,cortex and hippocampal tissue of the mice and measured the express of Aβ by ELISA,observed the deposition of Aβ plaque in the cortex and hippocampus of mice by immunofluorescence staining and compared the percentage of Aβ plaque in different parts using imageJ software,to study the changes of Aβ express in plasma,cortex and hippocampuse and the changes of Aβ plaque deposition in cortex and hippocampuse after chronic rapid eye movement sleep deprivation.Results:After chronic rapid eye movement sleep deprivation,the memory of pain in the APP/PS1 transgenic mice in the sleep deprivation group was significantly reduced in the passive avoidance text,the deposition of Aβ plaque in the cortex and hippocampal tissue was significantly increased,and the percentage of Aβ plaque in the cortex was significantly increased.Conclusion:Chronic rapid eye movement sleep deprivation aggravated memory impairment in APP/PS1 transgenic mice,and increased deposition of Aβ plaque in the hippocampus and cortex.The increased deposition of Aβ plaques in the cortex was more significant,this suggested that Aβ deposition in the cortex was closely related to the decreased cognitive function induced by chronic rapid eye movement sleep deprivation.