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Blood biomarkers indicate mild neuroaxonal injury and increased amyloid β production after transient hypoxia during breath-hold diving
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Department of Neurosurgery. Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Quanterix, Lexington, MA, USA,.
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2016 (English)In: Brain Injury, ISSN 0269-9052, E-ISSN 1362-301X, Vol. 30, no 10, 1226-1230 p.Article in journal (Refereed) Published
Abstract [en]

Objective: To determine whether transient hypoxia during breath-hold diving causes neuronal damage or dysfunction or alters amyloid metabolism as measured by certain blood biomarkers.

Design: Sixteen divers competing in the national Swedish championship in breath-hold diving and five age-matched healthy control subjects were included. Blood samples were collected at baseline and over a course of 3 days where the divers competed in static apnea (STA), dynamic apnea without fins (DYN1) and dynamic apnea with fins (DYN2).

Main outcomes: Biomarkers reflecting brain injury and amyloid metabolism were analysed in serum (S-100β, NFL) and plasma (T-tau, Aβ42) using immunochemical methods.

Results: Compared to divers’ baseline, Aβ42 increased after the first event of static apnea (p = 0.0006). T-tau increased (p = 0.001) in STA vs baseline and decreased after one of the dynamic events, DYN2 (p = 0.03). Further, T-tau correlated with the length of the apneic time during STA (ρ = 0.7226, p = 0.004) and during DYN1 (ρ = 0.66, p = 0.01).

Conclusion: The findings suggest that transient hypoxia may acutely increase the levels of Aβ42 and T-tau in plasma of healthy adults, further supporting that general hypoxia may cause mild neuronal dysfunction or damage and stimulate Aβ production.

Place, publisher, year, edition, pages
Taylor & Francis, 2016. Vol. 30, no 10, 1226-1230 p.
Keyword [en]
Amyloid, breath-hold diving, tau, hypoxia, blood biomarkers, neuroaxonal injury
National Category
Neurology
Identifiers
URN: urn:nbn:se:liu:diva-132561DOI: 10.1080/02699052.2016.1179792ISI: 000384324300009PubMedID: 27389622OAI: oai:DiVA.org:liu-132561DiVA: diva2:1046668
Available from: 2016-11-14 Created: 2016-11-14 Last updated: 2016-11-21Bibliographically approved

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