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How a molecule deletes neural chatter might help treat Angelman syndrome

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Researchers from the University of Tokyo reveal how the presynaptic Ube3a E3 ligase, a causal factor in Angelman syndrome, eliminates neural chatter. The study helps find a better drug target for the Angelman syndrome treatment.

involved in synaptic elimination during neural development and offer insights into developmental disorders such as Angelman syndrome.that affects neuronal development and causes physical and intellectual disabilities. In patients with Angelman syndrome, a gene called Ube3a does not function well, which prevents synapse elimination during development. On the other hand, abnormally high Ube3a leads to precocious synapse elimination and causes autism spectrum disorders.

His team probed the sensory neurons of the common fruitfly, Drosophila melanogaster, and successfully identified the Ube3a and its inner workings. That helped them reveal its role in synapse elimination.

 

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