Acute sleep deprivation increases serum levels of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in healthy young men.
OBJECTIVE
To investigate whether total sleep deprivation (TSD) affects circulating concentrations of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in humans. These factors are usually found in the cytoplasm of neurons and glia cells. Increasing concentrations of these factors in blood may be therefore indicative for either neuronal damage, impaired blood brain barrier function, or both. In addition, amyloid β (Aβ) peptides 1-42 and 1-40 were measured in plasma to calculate their ratio. A reduced plasma ratio of Aβ peptides 1-42 to 1-40 is considered an indirect measure of increased deposition of Aβ 1-42 peptide in the brain.


METHODS
Subjects participated in two conditions (including either 8-h of nocturnal sleep [22:30-06:30] or TSD). Fasting blood samples were drawn before and after sleep interventions (19:30 and 07:30, respectively).


METHODS
Sleep laboratory.


METHODS
15 healthy young men.


RESULTS
TSD increased morning serum levels of NSE (P = 0.002) and S-100B (P = 0.02) by approximately 20%, compared with values obtained after a night of sleep. In contrast, the ratio of Aβ peptides 1-42 to 1-40 did not differ between the sleep interventions.


CONCLUSIONS
Future studies in which both serum and cerebrospinal fluid are sampled after sleep loss should elucidate whether the increase in serum neuron-specific enolase and S100 calcium binding protein B is primarily caused by neuronal damage, impaired blood brain barrier function, or is just a consequence of increased gene expression in non-neuronal cells, such as leukocytes.
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Christian
C
Benedict
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Jonathan
J
Cedernaes
Molecular Geriatrics, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Vilmantas
V
Giedraitis
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Emil K
EK
Nilsson
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Pleunie S
PS
Hogenkamp
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Evelina
E
Vågesjö
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Sara
S
Massena
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Ulrika
U
Pettersson
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Gustaf
G
Christoffersson
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Mia
M
Phillipson
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Jan-Erik
JE
Broman
Molecular Geriatrics, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Lars
L
Lannfelt
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden ; UCL Institute of Neurology, Queen Square, London, UK.
Henrik
H
Zetterberg
Department of Neuroscience, Uppsala University, Uppsala, Sweden.
Helgi B
HB
Schiöth
D000208:Acute Disease; D016229:Amyloid beta-Peptides / Q000097:blood; D005215:Fasting / Q000097:blood; D064368:Healthy Volunteers; D006801:Humans; D008297:Male; D010446:Peptide Fragments / Q000097:blood; D010751:Phosphopyruvate Hydratase / Q000097:blood*; D009418:S100 Proteins / Q000097:blood*; D012890:Sleep / Q000502:physiology; D012892:Sleep Deprivation / Q000097:blood*; D013997:Time Factors; D055815:Young Adult
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; D009418:S100 Proteins; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42); D010751:Phosphopyruvate Hydratase
S100 calcium binding protein B; Sleep loss; amyloid beta; neuron-specific enolase; sleep