Current research explores the role of neuroligin mutations in patients with autism who have trouble sleeping, explains a blog post on BioMed Central.
ASD are typically diagnosed in humans between the ages 2 to 4, a period characterized by extensive activity-dependent neuronal remodeling. The pathogenesis of ASD has been proposed to depend on 2 mechanisms: abnormal cellular/synaptic growth and alterations in the balance between neuronal excitation/inhibition (E/I).
Neuroligins (Nlgns) are a family of post-synaptic cell adhesion molecules that are important for proper synaptic transmission, plasticity, and neuronal E/I balance. More importantly, the R451C missense mutation of neuroligin 3 (Nlgn3R451C), an X-linked gene, was identified in cases of ASD in humans. Recent work using rodent models demonstrated that neuroligin 3 is important for social interaction, vocal communication, as well as repetitive behavioural stereotypies, which are the key features of ASD. However, the role of neuroligin 3 in sleep regulation had not been examined until recently.
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