ArticleNature communications2026
Cross-species evidence for a developmental origin of adult hypersomnia with loss of synaptic adhesion molecules beat-Ia/CADM2.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Emerging genetics of sleep and circadian disorders.Current opinion in pediatrics · 2026Article
- Beat- and Side-family cell-surface molecules are expressed combinatorially in the partner neurons of the olfactory circuit in Drosophila.PLoS biology · 2026Article
- Cross-trait clustering of sub-threshold sleep genetic signals identifies EGR2 as a conserved regulator of sleep.bioRxiv : the preprint server for biology · 2026Article
- Meta-analysis of Cannabis Use Identifies Shared Genetic Loci with Sleep and Circadian Rhythms.medRxiv : the preprint server for health sciences · 2026Article
- Cell-specific variant-to-gene mapping identifies conserved neural and glial regulators of sleep.bioRxiv : the preprint server for biology · 2026Article
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Abstract
Idiopathic hypersomnia (IH) is a poorly understood sleep disorder characterized by excessive daytime sleepiness despite normal nighttime sleep. Combining human genomics with behavioral and mechanistic studies in fish and flies, we uncover a role for beat-Ia/CADM2, synaptic adhesion molecules of the immunoglobulin superfamily, in excessive sleepiness. Neuronal knockdown of Drosophila beat-Ia results in sleepy flies and loss of the vertebrate ortholog of beat-Ia, CADM2, results in sleepy fish. We delineate a developmental function for beat-Ia in synaptic elaboration of neuropeptide F (NPF) neurites projecting to the suboesophageal zone (SEZ) of the fly brain. Brain connectome and experimental evidence demonstrate these NPF outputs synapse onto a subpopulation of SEZ GABAergic neurons to stabilize arousal. NPF is the Drosophila homolog of vertebrate neuropeptide Y (NPY), and an NPY receptor agonist restores sleep to normal levels in zebrafish lacking CADM2. These findings point towards NPY modulation as a treatment target for human hypersomnia.
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