Ricardo Osorio, MD

"If we prove sleep to really have an effect on how Alzheimer presents and if we can actually prevent the onset, that would be the most interesting question to solve."

With an increasingly high number of adults suffering from dementia, understanding factors responsible for cognitive impairment is critical. Emerging evidence suggests that the sleep-wake cycle directly influences levels of cerebrospinal fluid (CSF) amyloid beta (Aβ) and tau concentrations—2 key pathological processes that have been extensively used as biomarkers of Alzheimer disease pathology.

In the last 5—7 years, data has shown that sleep disruption is not only a consequence of Alzheimer disease, but it’s also a risk factor, however, there are still many questions that remain unanswered.

sat down with Ricardo Osorio, MD, associate professor, department of psychiatry, NYU Langone, at the 24

 Congress of the European Sleep Research Society to speak about the relationship between poor sleep and Alzheimer disease and the questions that remain unanswered.

One of the most interesting questions Osorio hopes to solve is that if sleep is proven to have an effect on the presentation of Alzheimer, is it then possible to prevent the onset by enhancing sleep.  

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The associate professor at NYU Langone discussed several of the questions that remained unanswered about the relationship between sleep and Alzheimer disease.

Ricardo Osorio, MD: Unanswered Questions About the Relationship Between Sleep, Alzheimer Disease

“In the last 5&shy;—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."

 Congress of the European Sleep Research Society meeting in Basel, Switzerland, 

 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.

The associate professor at NYU Langone discussed emerging evidence that suggests that sleep disruption results in higher levels of markers associated with Alzheimer disease.

Ricardo Osorio, MD

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