Knockdown of the expression of OPN has been shown to mitigate ischemic brain injury in mice.[160] OPN is activated in CD11c‐positive microglia in AD, and inhibiting its production can reduce the number of pro‐inflammatory microglia, plaque formation, and atrophic neurites, thereby improving cognitive function.[161] Given its multifaceted roles, OPN is considered a potential therapeutic target, and future research may further investigate its applications in the treatment of bone and neural injuries. Here, SPP1 is linked to Alzheimer disease.