Insomnia is the most common sleep disorder, especially affecting individuals with neurodegenerative diseases. Humans with insomnia often expand the amount of time they spend in bed to compensate for inability to sleep. However, this mismatch of time in bed (high) with sleep ability (low) perpetuates insomnia symptoms. Cognitive Behavioral Therapy for Insomnia (CBT-I) is the first-line insomnia treatment. Sleep restriction – a key component of CBT-I – addresses this mismatch by restricting time in bed, leading to enhanced sleep drive and consolidation. We developed a Drosophila model for Sleep Restriction Therapy for insomnia, and validated its efficacy at improving sleep efficiency and continuity in short-sleeping Drosophila mutants. Following this finding, we expanded this therapy’s application to models of neurodegenerative disease in flies. We found that overexpression of human TDP-43, the protein deposited in inclusions in amyotrophic lateral sclerosis (ALS), caused profound sleep disturbances. Sleep Restriction Therapy rescued sleep deficits, causing efficient sleep without a change in total sleep duration. TDP-43 overexpressing flies undergoing Sleep Restriction Therapy also showed extended lifespan, indicating benefits from improved sleep to the overall health of the organism. Utilizing sleep behavior as a screening platform, we identified novel suppressors of TDP-43 toxicity poised to further elucidate disease processes.