The therapeutic hypothesis is derived exclusively from computational network proximity to IGF1 and synaptic dysfunction pathways, without experimental validation of effects on core AD pathologies including amyloid-β aggregation, tau phosphorylation, neuroinflammation, synaptic loss, or cognitive decline in transgenic AD mice (APP/PS1, 3xTg-AD, 5xFAD) or human AD-derived cellular models (iPSC neurons, brain organoids). This evidence concerns the gene IGF1 and Alzheimer disease.