This correlated with the amelioration of cognitive deficits and AD pathological changes, including the upregulation of hippocampal synaptic proteins, such as synapsin I (Syn1) and postsynaptic density protein 95 (PSD‐95), in addition to a decrease in the phosphorylation level of c‐Jun N‐terminal kinase (JNK) (Chen et al., 2017; Sun et al., 2019). Here, PROS1 is linked to Alzheimer disease.