CBLN1 tagged posts

The Genes, Neural Circuits behind Autism’s Impaired Sociability: ‘toggle switch’

The trans-synaptic GluRδ2-Cbln1-neurexin triad is essential for synapse formation

The trans-synaptic GluRδ2-Cbln1-neurexin triad is essential for synapse formation

BIDMC scientists determined how a gene linked to one common form of autism works in a specific population of brain cells to impair sociability. The research, published in the journal Nature, reveals the neurobiological control of sociability and could represent important first steps toward interventions for patients with autism. Anderson and colleagues focused on gene UBE3A, multiple copies of which causes a form of autism in humans (called isodicentric chromosome 15q).Conversely, the lack of this same gene in humans leads to a developmental disorder called Angelman’s syndrome, characterized by increased sociability...

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