1. Lau WKW, Leung MK, Zhang R. {{Hypofunctional connectivity between the posterior cingulate cortex and ventromedial prefrontal cortex in autism: Evidence from coordinate-based imaging meta-analysis}}. {Prog Neuropsychopharmacol Biol Psychiatry}. 2020; 103: 109986.
BACKGROUND: Underconnectivity in the posterior cingulate cortex (PCC) may be associated with a weakened ability to interpret social signals in autism spectrum disorder (ASD) and result in cognitive inflexibility – a hallmark feature of ASD. However, previous neuroimaging studies using resting-state functional magnetic resonance imaging in ASD reported inconsistent findings on functional connectivity of the PCC. This study investigated the aberrant resting-state functional connectivity of the PCC in ASD using multilevel kernel density analysis. METHODS: Online databases (MEDLINE/PubMed) were searched for PCC-based functional connectivity in ASD. Ten studies (501 subjects; 161 reported foci) met the inclusion criteria of this meta-analysis. RESULTS: We found one consistent and strong abnormal functional connectivity of ASD during the resting state, which was the hypoconnectivity between the PCC and ventromedial prefrontal cortex (VMPFC). Importantly, the Jackknife sensitivity analysis revealed that the VMPFC cluster was stably hypoconnected with the PCC in ASD (maximum spatial overlap rate: 100%). CONCLUSIONS: The reduced PCC-VMPFC functional coupling may provide an early insight into the effects of ASD on multiple dimensions of functioning, including higher-order cognitive and complex social functions.
Lien vers le texte intégral (Open Access ou abonnement)
2. Saad K, Abdallah AM, Abdel-Rahman AA, Al-Atram AA, Abdel-Raheem YF, Gad EF, Abo-Elela MGM, Elserogy YM, Elhoufey A, Nigm DA, Nagiub Abdelsalam EM, Alruwaili TAM. {{Polymorphism of interleukin-1β and interleukin-1 receptor antagonist genes in children with autism spectrum disorders}}. {Prog Neuropsychopharmacol Biol Psychiatry}. 2020; 103: 109999.
In this study, we first investigated interleukin-1 beta (IL-1β) and IL-1 receptor antagonist (IL-1RA) levels in a cohort of Egyptian children with autism spectrum disorder (ASD) and in healthy controls. Second, we examined the single-nucleotide polymorphisms (SNPs) at positions -31 and – 511 of the IL-1β gene promoter and IL1RA and assessed the association between IL1B and IL1RA polymorphisms with ASD. We examined IL1β promoter polymorphism at -511 (IL-1β-511) and – 31 (IL-1β-31) and IL1RA gene polymorphism in 80 children with ASD and 60 healthy children. The children with ASD had significantly higher levels of IL-1β and IL-1RA than the controls. The children with ASD also had significantly higher frequencies of homozygous (CC) and heterozygous (TC) genotype variants of IL-1β-511, and IL-1RA than the controls. Moreover, the frequency of the IL-1β-511 allele (C) was higher in the ASD group than in the controls (p = .001). The homozygous and heterozygous variants of IL-1RA allele II were also significantly higher in the ASD group than in the control group. There was no significant association between the IL-1β-31 genotype and autism classes. However, there were significant differences in the distribution of the IL-1RA heterogeneous genotype and allele II among children with severe autism. The inflammatory role of cytokines has been implicated in a variety of neuropsychiatric pathologies, including autism. Our data show alterations in the IL-1β system, with abnormally increased serum levels of IL-1β and IL-1RA in the children with ASD. Further, polymorphisms in the IL-1β-511 and IL-1RA genotype variants correlated positively with autism severity and behavioral abnormalities. IL-1β-511 and IL-1RA gene polymorphisms could impact ASD risk and may be used as potential biomarkers of ASD. Variations in the IL-1β and IL-1RA systems may have a role in the pathophysiology of ASD.
