Conclusions
cerebral AD, neuronal injury, hypoxia-ischemia
DISEASE, MINOR, PATHOLOGY, CARDIAC ARREST
In this study, the dynamics and prognostication capabilities of AD blood biomarkers (p-tau and Aβ) and markers of neural injury (NfL and t-tau) differed after cardiac arrest. In this case, the early increase of blood p-tau was not determined by the presence of cerebral AD pathology but dependent on the severity of the initial insult. Yet p-tau did not reflect ongoing and active neuronal injury, given the rapid clearance and diminished prognostic accuracy after 24 hours, which is better reflected by NfL. In contrast, delayed minor increases in Aβ peptides support activation of amyloidogenic processing in response to acute hypoxia-ischemia. This study highlights the importance of alternative disease mechanisms to understand the origin of temporal change of AD biomarkers in blood, as the manifestation and fluctuations of p-tau and Aβ in the bloodstream were not solely associated with Aβ plaques and neurofibrillary tau tangles.