Nevertheless, studies in AD remain limited.[43–45] Comprehensive bioinformatics analysis and experiments conducted by Yin et al unearthed significantly elevated CCNB2 expression levels in AD patients, which is consistent with our observations.[46]MELK, a member of the serine/threonine family of proteins, has been demonstrated to play a role in various cellular processes, including cell proliferation, apoptosis and cell cycle progression.[47,48] Apoptosis constitutes one of the pathogenic mechanisms underlying AD. This evidence concerns the gene MELK and Alzheimer disease.