Under serum exposure, treatment with CHIR99021 (a GSK3α/β inhibitor) significantly reduced the levels of phosphorylated and total GSK3α/β and p-tau, indicating that serum exposure induced p-tau and that the GSK3α/β-tau signaling pathway is crucial in AD pathogenesis, identifying it as a potential therapeutic pathway (Fig. 4a). Here, GSK3A is linked to Alzheimer disease.