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The abnormal accumulation of amyloid and tau protein leads to neurodegeneration in AD and related neurocognitive disorders. This comprehensive update reviews the evolving role of amyloid and tau PET in clinical practice (eg, diagnosis, management, challenges of reimbursement and workforce capacity), particularly in the setting of antiamyloid monoclonal antibody therapies.

AD is characterized by the accumulation of extracellular amyloid-β in the brain parenchyma and along the walls of cerebral blood vessels, leading to decreased CBF. CBF changes on ASL-MR could reflect clearance of amyloid-β on lecanemab therapy, raising the possibility that ASL-MR could serve as a tool for monitoring the neurovascular treatment response.