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Cross-species evidence for a developmental origin of adult hypersomnia with loss of synaptic adhesion molecules beat-Ia/CADM2

Cross-species studies show that loss of the synaptic adhesion molecules beat-Ia/CADM2 causes excessive sleepiness by disrupting development of wake-promoting NPF/NPY brain circuits. Targeting NPY signaling may offer treatment for human hypersomnia.

Kyla Mace
Amber Zimmerman
Matthew S. Kayser
ResearchOpen Access12 Jan 2026
Nature Communications

P: 1-18

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Cross-species evidence for a developmental origin of adult hypersomnia with loss of synaptic adhesion molecules beat-Ia/CADM2

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