Losing sleep with age.

Jacobson and Hoyer summarize experiments of Li et al.:

Humans spend approximately one-third of their lives asleep, but this is not distributed equally across their life span. Sleep quantity and quality decline as age advances, and insomnia and sleep fractionation are common in older people. Sleep is essential for vitality and health. At any age, chronic sleep deprivation causes a range of issues, including disrupted cognition and memory. Correspondingly, sleep complaints in older people are associated with increased risks of impaired physical and mental health and with mortality. Beyond evidence of degenerating subcortical nuclei in age-associated sleep disturbances, the underlying mechanisms remain unclear despite decades of awareness of the problem and its consequences...Li et al.report the hyperexcitability of hypocretin neurons as a core mechanism underlying sleep disruption in aged mice, explaining why sleep is punctuated by intruding wakefulness despite the loss of wake-promoting neurons.

A few clips from the Li et al. article: 

RATIONALE

We hypothesized that the decline in sleep quality could be due to malfunction of the neural circuits associated with sleep/wake control. It has been established that hypocretin/orexin (Hcrt/OX) neuronal activity is tightly associated with wakefulness and initiates and maintains the wake state. In this study, we investigated whether the intrinsic excitability of Hcrt neurons is altered, leading to a destabilized control of sleep/wake states during aging.

RESULTS

Aged mice exhibited sleep fragmentation and a significant loss of Hcrt neurons. Hcrt neurons manifested a more frequent firing pattern, driving wake bouts and disrupting sleep continuity in aged mice. Aged Hcrt neurons were capable of eliciting more prolonged wake bouts upon optogenetic stimulations. These results suggested that hyperexcitability of Hcrt neurons emerges with age. Patch clamp recording in genetically identified Hcrt neurons revealed distinct intrinsic properties between the young and aged groups. Aged Hcrt neurons were hyperexcitable with depolarized membrane potentials (RMPs) and a smaller difference between RMP and the firing threshold.

CONCLUSION

Aged mice exhibited sleep fragmentation and a significant loss of Hcrt neurons. Hcrt neurons manifested a more frequent firing pattern, driving wake bouts and disrupting sleep continuity in aged mice. Aged Hcrt neurons were capable of eliciting more prolonged wake bouts upon optogenetic stimulations. These results suggested that hyperexcitability of Hcrt neurons emerges with age. Patch clamp recording in genetically identified Hcrt neurons revealed distinct intrinsic properties between the young and aged groups. Aged Hcrt neurons were hyperexcitable with depolarized membrane potentials (RMPs) and a smaller difference between RMP and the firing threshold.