APP and Alzheimer disease: Previous investigation into the genetic foundations of Early Onset AD (EOAD) has yielded valuable insights into its pathophysiology, particularly regarding the roles of APP and presenilins in amyloid deposition.[14, 15, 16] Over the past few decades, Genome‐Wide Association Studies (GWAS) have significantly enriched and reshaped our understanding of the genetic landscape of AD.[17] Notably, various susceptibility loci have been identified, including members of the MS4A gene family,[18, 19, 20] in late‐onset AD (LOAD), which accounts for over 95% of AD cases.