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Sleep Deprivation Affects Tau Phosphorylation in Human Cerebrospinal Fluid
Author(s) -
Barthélemy Nicolas R.,
Liu Haiyan,
Lu William,
Kotzbauer Paul T.,
Bateman Randall J.,
Lucey Brendan P.
Publication year - 2020
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.25702
Subject(s) - cerebrospinal fluid , neurodegeneration , hyperphosphorylation , sleep (system call) , tau protein , sleep deprivation , alzheimer's disease , phosphorylation , neuroscience , medicine , tauopathy , glymphatic system , endocrinology , disease , psychology , chemistry , cognition , biochemistry , computer science , operating system
Tau hyperphosphorylation is an early step in tau‐mediated neurodegeneration and is associated with intracellular aggregation of tau as neurofibrillary tangles, neuronal and synaptic loss, and eventual cognitive dysfunction in Alzheimer disease. Sleep loss increases the cerebrospinal fluid concentration of amyloid‐β and tau. Using mass spectrometry, we measured tau and phosphorylated tau concentrations in serial samples of cerebrospinal fluid collected from participants who were sleep‐deprived, treated with sodium oxybate, or allowed to sleep normally. We found that sleep loss affected phosphorylated tau differently depending on the modified site. These findings suggest a mechanism for sleep loss to increase risk of Alzheimer disease. ANN NEUROL 2020;87:700–709