This is an exciting paper, which provides a possible mechanistic link between slow-wave neuronal activity during NREM sleep and pulsations in CSF flow. It offers a new insight into how sleep-related changes in neuronal activity potentially alter CSF dynamics via regulation of vascular tone. It will be interesting to see exactly how these findings integrate with glymphatic function and fluid flow through meningeal lymphatics. Interestingly, the Nedergaard lab and others have shown that arterial pulsation can drive interstitial fluid movement in the brain, and this paper suggests that that may occur as a result of changes in neuronal firing during sleep.
Despite my enthusiasm, it is important to first note that this was observed in a small number of healthy adults, and must be replicated by other groups. More importantly, any connection to Alzheimer's disease or Aβ clearance is strictly speculative, as no AD patients were examined in this study, and no measures of Aβ or other AD-related molecules were performed. The authors state this, and do speculate on this possibility briefly in the paper (which is appropriate), but many other media outlets are already reporting this finding as a breakthrough in our understanding of how the sleep clears toxins from the brain in AD. This study does not examine clearance of any substances from the brain, though it has clear implications for that process.
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Washington University School of Medicine
This is an exciting paper, which provides a possible mechanistic link between slow-wave neuronal activity during NREM sleep and pulsations in CSF flow. It offers a new insight into how sleep-related changes in neuronal activity potentially alter CSF dynamics via regulation of vascular tone. It will be interesting to see exactly how these findings integrate with glymphatic function and fluid flow through meningeal lymphatics. Interestingly, the Nedergaard lab and others have shown that arterial pulsation can drive interstitial fluid movement in the brain, and this paper suggests that that may occur as a result of changes in neuronal firing during sleep.
Despite my enthusiasm, it is important to first note that this was observed in a small number of healthy adults, and must be replicated by other groups. More importantly, any connection to Alzheimer's disease or Aβ clearance is strictly speculative, as no AD patients were examined in this study, and no measures of Aβ or other AD-related molecules were performed. The authors state this, and do speculate on this possibility briefly in the paper (which is appropriate), but many other media outlets are already reporting this finding as a breakthrough in our understanding of how the sleep clears toxins from the brain in AD. This study does not examine clearance of any substances from the brain, though it has clear implications for that process.
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