Therefore, in this study, we aimed to delineate the role of LRRK2 in reducing depression-related symptoms in a mouse model of mTBI and to determine whether Cu metabolism, glial cells and glutamate circuitry are involved in the underlying mechanisms by which the LRRK2 antagonist PF-475 exerts its antidepressant effect. This evidence concerns the gene LRRK2 and depressive symptom measurement.