CONCLUSIONS: Compared to other preclinical models, Cacng2 mutant mice uniquely combine a human-relevant genetic mutation with spontaneous absence seizures and quantifiable deficits in sustained attention. The model thus provides a powerful platform for investigating the neurobiological intersection of epilepsy and ADHD and for evaluating potential therapeutic interventions. Our results underscore the need to disentangle seizure-driven effects from genetically mediated comorbid cognitive deficits…
