Christoffer Rosén1, Hans Rosén2, Ulf Andreasson3, Daniel Bremell4, Rosemary Bremler5, Lars Hagberg6, Lars Rosengren7, Kaj Blennow8, Henrik Zetterberg9. 1. Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. Electronic address: christoffer.rosen@neuro.gu.se. 2. Institute of Clinical Neuroscience, Department of Neurology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: hans.rosen@neuro.gu.se. 3. Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. Electronic address: ulf.andreasson@neuro.gu.se. 4. Department of Infectious Medicine, Institute of Biomedicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: daniel.bremell@infect.gu.se. 5. Karlstad Hospital, Karlstad, Sweden. Electronic address: rosemarybremler@gmail.com. 6. Department of Infectious Medicine, Institute of Biomedicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: lars.hagberg@medfak.gu.se. 7. Institute of Clinical Neuroscience, Department of Neurology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: lars.rosengren@neuro.gu.se. 8. Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden. Electronic address: kaj.blennow@neuro.gu.se. 9. Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden; UCL Institute of Neurology, Queen Square, London WC1N 3BG, United Kingdom. Electronic address: henrik.zetterberg@clinchem.gu.se.
Abstract
AIM: The aim of this study was to investigate the levels of various cerebrospinal fluid (CSF) biomarkers related to neuronal damage, inflammation and amyloid β (Aβ) metabolism in patients resuscitated after an out-of-hospital cardiac arrest (CA). METHODS: CSF levels of neurofilament light protein (NFL), total tau (T-tau), hyperphosphorylated tau (P-tau), YKL-40, Aβ38, Aβ40, Aβ42, soluble amyloid precursor protein α and β (sAPPα and sAPPβ) were measured in 21 patients approximately two weeks after CA and in 21 age-matched neurologically healthy controls. The biomarker levels were also compared between patients with good and poor long-term clinical outcome according to Glasgow Outcome Scale (GOS), activities of daily living (ADL) and mini-mental state examination (MMSE), measuring neurologic function, daily functioning and cognitive function, respectively. RESULTS: Patients with CA had a very marked increase in the CSF levels of NFL, T-tau and YKL-40 as compared with controls. The levels were increased at about 1200, 700 and 100%, respectively. NFL and T-tau were significantly higher in patients with poor outcome according to all three outcome measures. Patients with poor outcome according to GOS and ADL had higher levels of YKL-40. Levels of Aβ38, Aβ40, Aβ42, sAPPα and sAPPβ were lower in patients with a low MMSE score. P-tau was not significantly altered. CONCLUSIONS: Biomarkers reflecting neuronal damage and inflammation, but not so much Aβ metabolism, were significantly altered in patients after a CA, and the changes were more pronounced in the groups with poor outcome. This calls for future larger studies to determine the prognostic potential of these biomarkers.
AIM: The aim of this study was to investigate the levels of various cerebrospinal fluid (CSF) biomarkers related to neuronal damage, inflammation and amyloid β (Aβ) metabolism in patients resuscitated after an out-of-hospital cardiac arrest (CA). METHODS: CSF levels of neurofilament light protein (NFL), total tau (T-tau), hyperphosphorylated tau (P-tau), YKL-40, Aβ38, Aβ40, Aβ42, soluble amyloid precursor protein α and β (sAPPα and sAPPβ) were measured in 21 patients approximately two weeks after CA and in 21 age-matched neurologically healthy controls. The biomarker levels were also compared between patients with good and poor long-term clinical outcome according to Glasgow Outcome Scale (GOS), activities of daily living (ADL) and mini-mental state examination (MMSE), measuring neurologic function, daily functioning and cognitive function, respectively. RESULTS:Patients with CA had a very marked increase in the CSF levels of NFL, T-tau and YKL-40 as compared with controls. The levels were increased at about 1200, 700 and 100%, respectively. NFL and T-tau were significantly higher in patients with poor outcome according to all three outcome measures. Patients with poor outcome according to GOS and ADL had higher levels of YKL-40. Levels of Aβ38, Aβ40, Aβ42, sAPPα and sAPPβ were lower in patients with a low MMSE score. P-tau was not significantly altered. CONCLUSIONS: Biomarkers reflecting neuronal damage and inflammation, but not so much Aβ metabolism, were significantly altered in patients after a CA, and the changes were more pronounced in the groups with poor outcome. This calls for future larger studies to determine the prognostic potential of these biomarkers.
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