Reader response: Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men
Vinod K.Gupta, Physician-Director, Migraine-Headache Institute, Gupta Medical Centre (New Delhi, India)
Submitted January 15, 2020
I read the article by Benedict et al.1 Across disease entities, vasopressin (AVP) has a well-defined adaptive function, particularly in relation to nocturnal sleep.2,3 Sleep analyses without considering the role of AVP remain incomplete.
A significant decrease in AVP in the Alzheimer disease (AD) brain has been found.4 AVP can potentiate hippocampal synaptic plasticity and dose-dependently prevent Aß(25-35)-induced long-term potentiation impairment, suggesting an important approach in the treatment of AD.4
AD-associated molecular pathways have been shown to be similar or analogous to those found in depression, including structural damage—i.e., hippocampal and frontal cortex atrophy.5 Rather than the acute model of induced-sleep deprivation used in this study,1 the chronic model of primary insomnia linked to depression-related real-time arousal and psychologic distress would have been far more representative for any analogy with AD.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Benedict C, Blennow K, Zetterberg H, Cedernaes J. Effects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men. Neurology 2020 Epub Jan 8.
Gupta VK. A clinical review of the adaptive role of vasopressin in migraine. Cephalalgia 1997;17:561–569.
Valiquette G. The neurohypophysis. Neurol Clin 1987;5:291–331.
Jing W, Guo F, Cheng L, Zhang JF, Qi JS. Arginine vasopressin prevents amyloid beta protein-induced impairment of long-term potentiation in rat hippocampus in vivo. Neurosci Lett 2009;450:306–310.
Rodrigues R, Petersen RB, Perry G. Parallels between major depressive disorder and Alzheimer's disease: role of oxidative stress and genetic vulnerability. Cell Mol Neurobiol 2014;34:925–949.
I read the article by Benedict et al.1 Across disease entities, vasopressin (AVP) has a well-defined adaptive function, particularly in relation to nocturnal sleep.2,3 Sleep analyses without considering the role of AVP remain incomplete.
A significant decrease in AVP in the Alzheimer disease (AD) brain has been found.4 AVP can potentiate hippocampal synaptic plasticity and dose-dependently prevent Aß(25-35)-induced long-term potentiation impairment, suggesting an important approach in the treatment of AD.4
AD-associated molecular pathways have been shown to be similar or analogous to those found in depression, including structural damage—i.e., hippocampal and frontal cortex atrophy.5 Rather than the acute model of induced-sleep deprivation used in this study,1 the chronic model of primary insomnia linked to depression-related real-time arousal and psychologic distress would have been far more representative for any analogy with AD.
Disclosure
The authors report no relevant disclosures. Contact journal@neurology.org for full disclosures.
References