Apaijai N, et al. - Whether PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor (PCSK9i) attenuates brain damage caused by cardiac ischemic/reperfusion (I/R) via diminishing microglial/astrocytic hyperactivation, β-amyloid aggregation, and loss of dendritic spine was investigated in this study performed on adult male rats. Subjects were grouped as control (n=4); PCSK9i without cardiac I/R (n=4); sham (n=4); and cardiac I/R (n=40), with further division of cardiac I/R rats into 4 subgroups (n=10/subgroup): vehicle; PCSK9i (10 μg/kg, IV) before ischemia; PCSK9i during ischemia; and PCSK9i at the onset of reperfusion. Researchers assessed microglial and astrocytic activities, β-amyloid aggravation, and dendritic spine density using brains removed at the end of cardiac I/R protocol. According to findings, cardiac I/R injury resulted in brain damage by activating microglial activity in the brain. Dendritic spine loss was prevented only by pretreatment with PCSK9i, via reduction of microglial activation and Aβ aggregation.