Sleep disturbances are among the risk factors associated with cognitive impairment

Will treating sleep disturbances reduce the risk of cognitive impairment? Probably. Are selfreported sleep disturbances the only significant risk factors associated with cognitive decline? Probably not. With the increasing incidence of cognitive impairment and dementia (Prince et al., 2016), it is crucial to identify and minimize all modifiable risk factors associated with cognitive decline. Kohn et al. (2019) describe several known risk factors for cognitive impairment, including inflammation, cardiometabolism, and mood disorders, but identified sleep disturbances to be the most notable risk factor associated with cognitive decline. There are known architectural sleep changes that occur in older adults by around the age of 60 years and may include decreased total sleep time, sleep efficiency, slow wave sleep, and rapid eye movement, in addition to an increase in time awake after sleep onset (WASO), number of arousals from sleep, and an increase in sleep latency. Despite the more frequent awakenings, healthy older adults usually are able to fall back asleep without great difficulty. In addition, phase advance may occur with aging, resulting in an earlier sleep onset and earlier morning awakenings as circadian rhythms change with age. This phenomenon is also called advanced sleep phase syndrome, and it not a disorder that necessarily requires treatment. While these changes are considered part of normal aging, there are other pathologic processes associated with aging that can affect sleep. They include medical and psychiatric comorbidities, substance use, and medications, such as diuretics, which may interfere with sleep. The two most common sleep disorders in older adults include obstructive sleep apnea (OSA) and insomnia disorder. The findings described in the paper by Kohn et al. (2019) focus on self-reported sleep disturbances. This would include excessive daytime sleepiness in the case of OSA, and increased WASO and decreased sleep efficiency in the case of insomnia disorder. Therefore, physicians should screen for these particular conditions and provide treatment accordingly. Behavioral treatments for insomnia are recommended as first-line treatment for insomnia (Qaseem et al., 2016), and we have learned that older adults with depression and insomnia have a preference for behavioral interventions over pharmacotherapy for the treatment of both depression and sleep disturbances (Gebara et al., 2019). Examples of learning-based approaches include cognitive behavioral therapy for insomnia (CBT-I) and brief behavioral treatment for insomnia (Buysse et al., 2011). CBT-I has the strongest evidence for treating insomnia (Wilson et al., 2010). These behavioral interventions focus on the principles of sleep restriction and stimulus control. Mechanisms associated with sleep disturbances that may contribute to cognitive decline are described by Yaffe et al. (2014). Sleep disturbances may affect amyloid-β deposition, increase neuroinflammation, and change synaptic plasticity. Most notably, sleep duration (too short or too long), sleep fragmentation, and sleep-disordered breathing (through hypoxia and sleep fragmentation) seem to increase the risk of cognitive impairment. The relationship between sleep and cognitive impairment may be bidirectional, with disruptions in the sleep–wake cycle being a manifestation of an underlying neurodegenerative process. Regardless of etiology, there appears to be a link between sleep disturbances and cognitive decline. While it is common to manage cardiometabolic and vascular risk factors for cognitive decline in primary care, sleep disturbances are frequently overlooked despite the fact that they affectmore than half of older adults. One of the reasons may be because it can be challenging to distinguish between normal aging-related sleep changes and pathologic changes that require intervention. Kohn et al. (2019) discuss some proposed mechanisms through which sleep disturbances are associated with cognitive decline and dementia including the effects of cardiometabolic risk factors and those of hypertension, specifically on cerebral microvasculature and white matter integrity. This highlights the need for patient education about healthy lifestyle behaviors and adherence to cardiometabolic medications to preserve cognition. Providers must emphasize the importance of medication compliance with all medications, especially antihypertensive and lipid-lowering agents. Given that all participants in this study had premorbid hypertension, participants may have been enriched to experience cognitive impairment. International Psychogeriatrics (2020), 32:7, 791–792 © International Psychogeriatric Association 2020