The neurotoxic effect occurs through the activation of caspases and/or suppression of ApoER2 expression.[16,17] In addition, silencing PCSK9 in AD mice models led to improved memory functions, reduced Aβ plaque deposition and attenuated neuroinflammation.[18] Moreover, elevated PCSK9 levels have been detected in the cerebrospinal fluid of AD patients.[19] However, the exact relationship between PCSK9 and AD remains unclear and requires further investigation. This evidence concerns the gene LRP8 and Alzheimer disease.