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Search: (L773:2168 6149 OR L773:2168 6157) pers:(Lantero Rodriguez Juan) > Alzheimer Disease B...

  • Ashton, Nicholas J.University of Gothenburg,Gothenburg University,Göteborgs universitet,Wallenberg Centre for Molecular and Translational Medicine,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,South London and Maudsley NHS Foundation Trust,King's College London,Sahlgrenska Academy (author)

Alzheimer Disease Blood Biomarkers in Patients With Out-of-Hospital Cardiac Arrest

  • Article/chapterEnglish2023

Publisher, publication year, extent ...

  • 2023-03-06
  • American Medical Association (AMA),2023

Numbers

  • LIBRIS-ID:oai:gup.ub.gu.se/326441
  • https://gup.ub.gu.se/publication/326441URI
  • https://doi.org/10.1001/jamaneurol.2023.0050DOI
  • https://lup.lub.lu.se/record/92408692-1d5c-4b29-8d52-06b02cbcbb1aURI

Supplementary language notes

  • Language:English

Part of subdatabase

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • IMPORTANCE Blood phosphorylated tau (p-tau) and amyloid-13 peptides (A13) are promising peripheral biomarkers of Alzheimer disease (AD) pathology. However, their potential alterations due to alternative mechanisms, such as hypoxia in patients resuscitated from cardiac arrest, are not known. OBJECTIVE To evaluate whether the levels and trajectories of blood p-tau, A1342, and A1340 following cardiac arrest, in comparison with neural injury markers neurofilament light (NfL) and total tau (t-tau), can be used for neurological prognostication following cardiac arrest.DESIGN, SETTING, AND PARTICIPANTS This prospective clinical biobank study used data from the randomized Target Temperature Management After Out-of-Hospital Cardiac Arrest (TTM) trial. Unconscious patients with cardiac arrest of presumed cardiac origin were included between November 11, 2010, and January 10, 2013, from 29 international sites. Serum analysis for serum NfL and t-tau were performed between August 1 and August 23, 2017. Serum p-tau, A1342, and A1340 were analyzed between July 1 and July 15, 2021, and between May 13 and May 25, 2022. A total of 717 participants from the TTM cohort were examined: an initial discovery subset (n = 80) and a validation subset. Both subsets were evenly distributed for good and poor neurological outcome after cardiac arrest.EXPOSURES Serum p-tau, A1342, and A1340 concentrations using single molecule array technology. Serum levels of NfL and t-tau were included as comparators.MAIN OUTCOMES AND MEASURES Blood biomarker levels at 24 hours, 48 hours, and 72 hours after cardiac arrest. Poor neurologic outcome at 6-month follow-up, defined according to the cerebral performance category scale as category 3 (severe cerebral disability), 4 (coma), or 5 (brain death).RESULTS This study included 717 participants (137 [19.1%] female and 580 male [80.9%]; mean [SD] age, 63.9 [13.5] years) who experienced out-of-hospital cardiac arrest. Significantly elevated serum p-tau levels were observed at 24 hours, 48 hours, and 72 hours in cardiac arrest patients with poor neurological outcome. The magnitude and prognostication of the change was greater at 24 hours (area under the receiver operating characteristic curve [AUC], 0.96; 95% CI, 0.95-0.97), which was similar to NfL (AUC, 0.94; 95% CI, 0.92-0.96). However, at later time points, p-tau levels decreased and were weakly associated with neurological outcome. In contrast, NfL and t-tau maintained high diagnostic accuracies, even 72 hours after cardiac arrest. Serum A1342 and A1340 concentrations increased over time in most patients but were only weakly associated with neurological outcome.CONCLUSIONS AND RELEVANCE In this case-control study, blood biomarkers indicative of AD pathology demonstrated different dynamics of change after cardiac arrest. The increase of p-tau at 24 hours after cardiac arrest suggests a rapid secretion from the interstitial fluid following hypoxic-ischemic brain injury rather than ongoing neuronal injury like NfL or t-tau. In contrast, delayed increases of A13 peptides after cardiac arrest indicate activation of amyloidogenic processing in response to ischemia.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Moseby-Knappe, MarionLund University,Lunds universitet,Neurologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Brain Injury After Cardiac Arrest,Forskargrupper vid Lunds universitet,Neurologiska skador vid akut aortadissektion typ A,Neurology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine,Lund University Research Groups,Neurological injury in acute type A aortic dissection,Skåne University Hospital(Swepub:lu)med-mmy (author)
  • Lessa Benedet, AndréaGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Sahlgrenska Academy(Swepub:gu)xlesan (author)
  • Grötschel, Lana,1993Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Sahlgrenska Academy(Swepub:gu)xgrotl (author)
  • Lantero Rodriguez, JuanGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Sahlgrenska Academy(Swepub:gu)xrodri (author)
  • Karikari, ThomasGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Sahlgrenska Academy,McGill University Research Centre for Studies in Aging(Swepub:gu)xkarit (author)
  • Hassager, C.Copenhagen University Hospital (author)
  • Wise, M. P.University Hospital of Wales (author)
  • Stammet, P.University of Luxembourg,Centre Hospitalier de Luxembourg (author)
  • Kjaergaard, J.Copenhagen University Hospital (author)
  • Friberg, HansLund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Centrum för hjärtstopp,Forskargrupper vid Lunds universitet,SWECRIT,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Center for cardiac arrest,Lund University Research Groups,Helsingborg Hospital(Swepub:lu)efor-hfr (author)
  • Nielsen, NiklasLund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Kliniska Vetenskaper, Helsingborg,Institutionen för kliniska vetenskaper, Lund,Centrum för hjärtstopp,Forskargrupper vid Lunds universitet,SEBRA Sepsis and Bacterial Resistance Alliance,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Clinical Sciences, Helsingborg,Department of Clinical Sciences, Lund,Center for cardiac arrest,Lund University Research Groups,Helsingborg Hospital(Swepub:lu)med-nni (author)
  • Cronberg, TobiasLund University,Lunds universitet,Neurologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Centrum för hjärtstopp,Forskargrupper vid Lunds universitet,Brain Injury After Cardiac Arrest,Neurology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine,Center for cardiac arrest,Lund University Research Groups,Skåne University Hospital(Swepub:lu)efor-tcr (author)
  • Zetterberg, Henrik,1973Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,University College London,Sahlgrenska University Hospital,Sahlgrenska Academy(Swepub:gu)xzethe (author)
  • Blennow, Kaj,1958Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry,Sahlgrenska University Hospital,Sahlgrenska Academy(Swepub:lu)med-kbw (author)
  • Göteborgs universitetWallenberg Centre for Molecular and Translational Medicine (creator_code:org_t)

Related titles

  • In:Jama Neurology: American Medical Association (AMA)80:4, s. 388-3962168-6149

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