CBT-I fails to improve cognitive performance or amyloid beta deposition in older adults with insomnia by one year

Sleep disturbances, particularly insomnia, are increasingly recognized as a significant risk factor for Alzheimer's disease (AD), potentially preceding overt cognitive decline. Accumulation of beta-amyloid (Aβ) plaques is a hallmark of AD pathology. While effective for sleep, it has been unclear whether non-pharmacological interventions like Cognitive Behavioral Therapy for Insomnia (CBT-I) could mitigate AD progression by influencing cognitive function or Aβ burden in at-risk older adults.

This randomized controlled trial enrolled 200 cognitively normal older adults experiencing insomnia symptoms. Participants were randomized into either a CBT-I treatment group (n = 100) or a control group (n = 100). Cognitive performance was assessed at baseline, 6-weeks, and 1-year. A subsample (n = 50) also underwent assessment for Aβ burden. The CBT-I intervention involved weekly sessions for the first 4 weeks, followed by biweekly sessions for the next 4 weeks, totaling an 8-week treatment phase.

The study found no significant differences between the CBT-I and control groups in the change of cognitive performance over one year. Specifically, for speed of information processing, the mean difference was 0.017 (95% CI, -0.1036 to 0.1376; p = 0.78). Executive function showed a mean difference of -0.0881 (95% CI, -0.2945 to 0.1182; p = 0.40), and memory had a mean difference of 0.4068 (95% CI, -2.3965 to 3.2101; p = 0.77).

No group differences were observed in Aβ deposition in the subsample of 50 participants. These results indicate that, within a one-year timeframe, CBT-I did not demonstrate a measurable impact on key cognitive domains or the accumulation of amyloid-beta in the brain.