Experimental studies in ethanol-treated murine models demonstrate that increased cerebellar Cer(d18:1/26:2) levels induce microglial hyperactivation via TLR4-mediated NF-κB signaling (36), while accumulation of pro-apoptotic Cer (d18:1/26:2) showed strong association with synaptic degeneration, recapitulating pathological features seen in Alzheimer’s disease (37). Here, CBLN1 is linked to early-onset autosomal dominant Alzheimer disease.