Eteleeb et al. integrated transcriptomic, proteomic, metabolomic, and lipidomic profiles with clinical and neuropathological data and identified four molecular AD profiles; one subtype displayed pronounced synaptic downregulation, astrocyte enrichment, neurotransmitter loss, and worse outcomes, all replicated across independent cohorts, with SNCA, SNAP25, GFAP, and CLU emerging as markers and single-nucleus RNA-seq revealing astrocytes and endothelial cells as key drivers [37]. The gene discussed is CLU; the disease is Alzheimer disease.