Association between the cerebral blood transit times, amyloid-β pathology and cognitive decline in non-dementia adults

Motivation: Despite increasing recognition of vascular injury's significance in AD pathogenesis, its impact on Alzheimer's disease (AD) progression remains obscure. Goal(s): We tested the hypothesis that cerebrovascular dysfunction, manifested as prolonged blood transit times, could accelerate amyloid-β (Aβ) deposition and thereby hasten cognitive decline. Approach: Employing blood-oxygenation-level-dependent (BOLD) signal delay analysis to assess cerebrovascular function, this study aimed to explore the relationships between cerebral blood transit times, amyloid-β (Aβ) pathology, and cognition in non-demented adults. Results: We found that prolonged blood transit times were significantly related to Aβ deposition and positively synergized with Aβ pathology in accelerating cognitive decline. Impact: This study highlights the role of prolonged blood transit times in AD progression, linking cerebrovascular dysfunction with Aβ pathology and cognitive decline.