Acute social isolation evokes midbrain craving responses similar to hunger.
Targeted long-read sequencing identifies missing disease-causing variation.
Modeling flexible behavior in childhood to adulthood shows age-dependent learning mechanisms and less optimal learning in autism in each age group.
Alexithymia in autism: Cross-sectional and longitudinal associations with social-communication difficulties, anxiety and depression symptoms.
A Conversation with SFARI Investigators Peter Kind and Loren Frank
Peter Kind and Loren Frank discuss their work using SFARI’s genetic rat models and their views on how these models will aid autism research.
Phenotyping sleep
Emmanuel Mignot discussed sleep biology as well as sleep disorders and their impact. He presented a link to what is known on the genetics of sleep and sleep disorders. He emphasized the need for large scale objective sleep recording studies with genomic and proteomic analysis to better understand the molecular pathways regulating sleep and circadian biology.
Emmanuel Mignot, M.D., Ph.D.
Emmanuel Mignot is the Craig Reynolds Professor of Sleep Medicine at Stanford University. He discovered that human narcolepsy is caused by an autoimmune loss of approximately 20,000 hypothalamic neurons secreting the wake-promoting peptide hypocretin (also known as orexin). He also identified HLA-DQB1*06:02 and T-cell receptor genes as major susceptibility genes, which act together to promote a selective autoimmune process triggered by influenza A. Mignot has received numerous awards and is a member of the National Academy of Sciences and the National Academy of Medicine.
Dissecting the phenotypic heterogeneity in sensory features in autism spectrum disorder: A factor mixture modelling approach.
Intrinsic excitation-inhibition imbalance affects medial prefrontal cortex differently in autistic men versus women.
Neuronal activity-dependent chromatin remodeling in autism
Neuronal activity triggers the expression of new genes that play a critical role in aspects of neural development and cognitive function. Building on evidence suggesting links between a class of ASD susceptibility loci (i.e., subunits of the BAF chromatin remodeling complex) and this form of gene regulation, Michael Greenberg and colleagues seek to determine whether disruption in neuronal activity-responsive chromatin remodeling underlies the effects of these ASD mutations.
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