The associate professor at NYU Langone discussed emerging evidence that suggests that sleep disruption results in higher levels of markers associated with Alzheimer disease.
“In the last 5­—7 years we have new data that shows that sleep disruption is not only a consequence of Alzheimer, but it’s also a risk factor."
At the 24th Congress of the European Sleep Research Society meeting in Basel, Switzerland, NeurologyLive sat down with Ricardo Osorio, MD, associate professor, department of psychiatry, NYU Langone, to discuss the relationship between sleep disruption and Alzheimer disease.
Emerging evidence suggests that the sleep-wake cycle directly influences levels of cerebrospinal fluid (CSF) amyloid beta (Aβ) and tau concentrations. Specifically, Osorio explains that low NREM stage 3 slow wave activity is associated with high CSF Aβ, while disruption of slow wave sleep results in an increase in CSF Aβ peptides. The data reveals that sleep disruptions result in higher levels of markers associated with Alzheimer disease, increase CNS oxidative stress and disrupt clearance of Alzheimer-promoting Aβ peptides. Unlike Aβ, associations between poor slow wave sleep and tau have not been observed, which suggest that disruption in other sleep oscillations could potentially be linked to tau pathology.
Osorio concludes that enhancing sleep can help in lowering the risk or reversing the signs of accelerated cognitive aging, Alzheimer disease or other neurodegenerative diseases and opens a new path of research to be explored.