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Association of amyloid load uptake and cerebral blood flow in non‐Alzheimer's disease dementia and mild cognitive impairment

Fibrillary beta amyloid deposits and cerebral hypoperfusion are upstream and downstream pathological features in demented individuals respectively. Asymptomatic amyloid plaque deposition begins and becomes saturated way before cerebral structural and metabolic changes in the course of Alzheimer’s disease dementia, and their relationships been vigorously studied. However, the relationship of amyloid load and cerebral functions in non‐AD dementia is under‐investigated. This study aims to investigate the correlation between plaque deposition and cerebral blood flow (CBF) in non‐AD demented individuals.