Plasma β amyloid and impaired CO2-induced cerebral vasomotor reactivity

Amyloid β (Aβ) may disturb cerebral autoregulation by damaging the wall of small cerebral blood vessels and by direct negative vasoactive properties. We assessed whether previous and concurrent plasma Aβ1–40 and Aβ1–42 levels were associated with an impaired CO2-induced cerebral vasomotor response. In the longitudinal population-based Rotterdam Study we measured plasma Aβ levels and cerebral vasomotor reactivity to hypercapnia with transcranial Doppler ultrasonography (TCD) in 441 people, aged 60–90 years. We performed age and sex adjusted logistic regression analysis. Plasma Aβ levels assessed on average 6.5-year before TCD were linearly associated with an impaired CO2-induced cerebral vasomotor response (odds ratio 1.48 (95%CI 1.19;1.84) per standard deviation increase in Aβ1–40, and 1.36 (95%CI 1.09;1.70) per standard deviation increase in Aβ1–42). Such an association was not present for Aβ assessed concurrently with the TCD measurement. Persons whose plasma Aβ1–40 levels had decreased in the 6.5-year period preceding TCD measurements were more likely to have an impaired CO2-induced vasomotor reactivity. Overall our observations are most compatible with plasma Aβ levels representing vascular Aβ deposits years later resulting in impaired CO2-induced vasomotor reactivity.