Unravelling the cellular and molecular mechanisms of the relationship between behavioral and cognitive impairment during the preclinical and prodromal phases of dementia will aid in delineating the role of amyloid deposition, tau accumulation and other related mechanisms in the trajectory of MBI, and pave the way for future advancements in personalized and targeted preventive and therapeutic strategies. The gene discussed is MAPT; the disease is Cognitive impairment.