ABSTRACT NUMBER: ESOC2026A2188 LONG-TERM INFLAMMATORY, FUNCTIONAL, AND ANATOMICAL DEFICITS AFTER FMCAO-INDUCED ISCHAEMIC STROKE IN MICE

Abstract Background and aims Stroke is a leading cause of disability; however, long-term effects of ischaemic stroke on cellular, cognitive, functional, and immunological processes remain poorly understood because well-characterised animal models capturing these chronic changes are lacking. To address this gap, we conducted a comprehensive experimental study assessing functional, anatomical, and inflammatory changes in a long-term survival mouse model of ischaemic stroke at 1, 3, and 6 months post-stroke. Methods C57bl/6 mice underwent sham-surgery or filamentous-middle-cerebral-artery-occlusion (fMCAo) and were monitored up to six months. Neurological deficits were measured longitudinally using neurological-behavioural tests. MRI scans were performed at 24 hours, 1, 3, and 6 months post-intervention. Inflammatory markers were studied in blood, CSF, and brain tissue via flow cytometry (FACS) 1, 3, and 6 months after intervention. Results fMCAo animals showed sustained neurological impairment at 1, 3, and 6 months post-stroke. While infarct volume decreased over time, MRI revealed significant (p<0.01) ipsilateral hemispheric atrophy compared to sham controls. FACS analysis revealed significant elevations of inflammatory cells e.g., microglia, CD45+ cells in brain tissue and in CSF one month after fMCAo, while we see no significant inflammatory changes in blood at any time-point. We found significantly (p<0.01) elevated monocytes in brain tissue one and six months post-intervention. At six months, CD19+ cells were significantly (p<0.05) elevated in CSF compared to sham controls. Conclusions In conclusion, fMCAo leads to sustained neurological deficits and brain tissue atrophy. Inflammatory changes in brain and CSF peak around 30 days post-stroke but persist in CSF and brain even 6 months thereafter. Conflict of interest Daria Fode: nothing to disclose