Chronobiology in Adulthood Autism Spectrum Disorder

Thursday, May 11, 2017: 5:30 PM-7:00 PM
Golden Gate Ballroom (Marriott Marquis Hotel)
P. Ballester-Navarro1,2, M. J. Martínez3, A. Javaloyes Sanchís4, N. Fernández Cogollor5, P. Gázquez Galera6 and A. M. Peiró2,7, (1)Hospital General Universitario de Alicante, Alicante, Spain, (2)Clinical Pharmacology, Organic Chemistry and Pediatrics, Universidad Miguel Hernández, Alicante, Spain, (3)Universidad de Murcia, Murcia, Spain, (4)EDUCATEA, Autism supporting living center, Alicante, Spain, (5)APNAV-ANGEL RIVIERE Autism supporting living center, Valencia, Spain, (6)Centro Infanta Leonor, Autism Support Living Center, Alicante, Spain, (7)Clinical Pharmacology, Hospital General Universitario de Alicante, Alicante, Spain

Sleep disorders can occur in up to the 80% of people with Autism Spectrum Disorder (ASD). The evidence behind the contribution of sleep circadian rhythms and molecular mechanisms involving clock genes and melatonin route in ASD is very limited.

Objectives:  Analyze the Circadian Rhythm sleep disorders (CRSD) in adults with ASD with Ambulatory Circadian Monitoring and their relationship with SNPs in ASMT, Per1, Npas 2, and MTNR1Agenes.

Methods:  A total of 92 subjects were enrolled on a prospective study to record sleep with Ambulatory Circadian Monitoring (24 hours for a week). Circadian rhythms (CR´s) were recorded and characterized by nonparametric indexes and sleep parameters were calculated. A subtotal of 51 subjects participated in a genetic substudy of SNPs from ASMT, Per1, Npas 2, and MTNR1Agenes. Statistical analysis was performed using GraphPad Prism 5.0.

Results: ASD patients had significantly major total sleep time, sleep onset latency, num. awakenings, WASO and lower SE compared to controls with significant differences of Sleep CR´s along 24 h ACM determination. The genetic substudy found significant differences (p< 0.05) in the recessive genetic model from rs5989681 and overdominant genetic model of rs6416892 and rs885747 when compared the genotype and SOL.

Conclusions:  This data suggest that ASD group sleep parameters and CR chronobiology could indicate the presence of CRSD in the ASD population. Apparently, there is a relationship between SOL and SNPs in genes Per1 and ASMT, but further genetic analysis increasing the study sample is required. Improving knowledge in this area is important for developing a model of sleep in ASD and targeting interventions.