Introduction
hypoxic-ischemic brain injury, brain injury
ALZHEIMER DISEASE (AD), NEURODEGENERATIVE DISORDERS, CARDIAC ARREST, PATHOPHYSIOLOGY, NEUROFIBRILLARY TANGLES, HYPOXIC-ISCHEMIC BRAIN INJURY
Extracellular amyloid-β (Aβ) plaques and neurofibrillary tangles composed of phosphorylated tau (p-tau) are the key protein signatures of a brain with Alzheimer disease (AD). Aβ peptides (Aβ42 and Aβ40) and p-tau can be quantified in cerebrospinal fluid (CSF) and, more recently, in blood, where both biomarkers show high accuracy in determining underlying AD brain pathologyIn addition to AD and other neurodegenerative disorders, blood biomarkers are also warranted in prognostication in unconscious patients experiencing hypoxic-ischemic brain injury following cardiac arrest. Current guidelines recommend a multimodal approach in the prediction of outcome after cardiac arrest,In the present study, we evaluated whether serum p-tau, Aβ42, Aβ40, and Aβ42/40 ratio, the most specific biomarkers for AD pathophysiology in blood, had altered levels after cardiac arrest. Furthermore, we examined if these biomarkers were associated with the severity of neurological outcome and compared their longitudinal trajectories (24 to 72 hours after cardiac arrest) to biomarkers of brain injury after cardiac arrest, namely NfL and t-tau.