In summary, the data obtained from the treatment of cerebral organoids by tramiprosate revealed that: (i) it was endogenously metabolized into SPA in cerebral organoids, (ii) it increased the concentration of cholesteryl ester and decreases the level of carnitines specifically in ApoE ε4/ε4 organoids, (iii) it increased the level of AD-related proteins involved in lipid transport and stimulated neurogenesis, and (iv) ApoE ε4/ε4 organoids treated with tramiprosate showed a specific decrease of P-ERK1/2 signaling levels. Here, APOE is linked to Alzheimer disease.