RESUMEN
Regardless of the nature of its operationalization, frailty has significant negative consequences for the person concerned and the community. Even if a generally accepted definition of frailty is still missing, there is no doubt about the existence of this phenomenon. Pathophysiologically, a dysfunctional interaction between multiple complex systems is discussed. Therapeutic interventions show that frailty is a dynamic state that can be improved. The pathophysiological characteristics of frailty and sleep disturbances show numerous similarities. In addition, the risk of frailty is increased in individuals with sleep disturbances. As the majority of sleep disorders can usually be well treated, screening for sleep disorders should be integrated into a comprehensive concept of management of frailty.
RESUMEN
Aging is associated with changes in sleep structure and cerebral deposition of amyloid beta and tau proteins. Sleep disturbances precede the onset of dementia by years. Comorbid sleep disorders, such as insomnia and sleep-disordered breathing, a family history of dementia and epigenetic factors can contribute to the development of dementia. This article explores the question of the interaction between sleep and dementia based on the existing literature. Alterations caused by slow wave sleep lead to changes in the glymphatic clearance of amyloid beta, tau proteins and other proteins. Transient and chronic sleep disorders cause disturbances in the brain areas responsible for cognition and behavior. Sleep-regulating brain areas are the first to be affected in the neurodegenerative process and accelerate the risk of dementia. Circadian age-related changes in amyloid beta and tau proteins affect the amount and depth of sleep and vice versa. Amyloid beta in cerebrospinal fluid shows an inverse correlation with sleep. Orexins modulate amyloid beta and sleep.