Abstract Number: Esoc2026a2204 Serum Brain-Derived Tau in Moyamoya Angiopathy: A Case–control Study of Associations With Cognitive Impairment

Abstract Background and aims Brain-derived tau (BD-tau) is a sensitive blood-based biomarker of neuronal injury in acute ischemic stroke; but its relevance in conditions characterized by chronic cerebral hypoperfusion remains unclear. Moyamoya angiopathy (MMA) is a progressive steno-occlusive disorder causing regional cerebral hypoperfusion, impaired vasomotor reserve, and heterogenous clinical phenotypes, including cognitive impairment, complicating risk stratification. Biomarkers reflecting hypoperfusion-related neuronal injury may complement imaging and clinical assessment in neurosurgical decision- making. We investigated serum BD-tau levels in MMA patients and healthy controls and explored relations with cognitive performance. Methods This cross-sectional, register-based case-control study included MMA patients without recent stroke (n = 37) and healthy controls (n = 14). Serum total BD-tau levels were compared using Mann-Whitney U test. MMA patients underwent comprehensive neuropsychological assessment across nine cognitive domains. A Global Cognitive Impairment Index (GCII) was calculated as the proportion of domains with at least one test score ≥1 standard deviation below normative means. Associations between BD-tau and GCII were assessed using Spearman´s rank correlation. Results Median serum BD-tau levels were 12.38 9.40–14.96 pg/mL in the MMA group and 9.97 9.27–13.77 pg/mL in the control group, without significant between-group difference (p = 0.263). Within the MMA group, BD-tau levels showed no significant correlation with GCII (p = 0.061). Conclusions Serum BD-tau levels were not elevated in MMA patients and were not associated with global impairment. Despite small sample size, these findings suggest limited general utility of BD-tau in MMA, though its potential in selected subgroups warrants further investigation in larger cohorts. Conflict of interest Jesper Sømark: nothing to disclose. Mona Skjelland: non-personal research grants from South-Eastern Norway Regional Health Authority (2024). Bente Halvorsen: is an SAB member in CircM, Linkøping, Sweden and is an evaluator in MH panel, Swedish Research council.. Thor Ueland: nothing to disclose.Vigdis Bjerkeli: nothing to disclose. Pål Aukrust: nothing to disclose. Tonje Nordenmark: nothing to disclose. Markus K.H. Wiedmann: nothing to disclose. Anne Hege Aamodt: has received personal fees for lectures/advisory boards; Novartis, Abbvis, TEVA, Roche, Lundbeck, Pfizer, Boehringer Ingelheim, non-personal research grants from Norwegian National Association for Public Health, South-Eastern Norway regional Health Authority, Odd Fellow, National Program for Clinical Treatment Research in the Specialist Health Service (KLINBEFORSK), EU, Boehringer Ingelheim, Medtronic, BMS. Figure 1 - belongs to Conclusions