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Amyloid beta (Abeta) 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 Abeta(1-40) and Abeta(1-42) levels were associated with an impaired CO2-induced cerebral vasomotor response. In the longitudinal population-based Rotterdam Study we measured plasma Abeta 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 Abeta 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 Abeta(1-40), and 1.36 (95%CI 1.09;1.70) per standard deviation increase in Abeta(1-42)). Such an association was not present for Abeta assessed concurrently with the TCD measurement. Persons whose plasma Abeta(1-40) 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 Abeta levels representing vascular Abeta deposits years later resulting in impaired CO2-induced vasomotor reactivity.

Original publication




Journal article


Neurobiology of aging

Publication Date





707 - 712


Department of Epidemiology and Biostatistics, Erasmus MC, Erasmus University Medical Center, PO Box 1738, 3000 Rotterdam, The Netherlands.


Brain, Vasomotor System, Humans, Carbon Dioxide, Ultrasonography, Doppler, Transcranial, Cohort Studies, Follow-Up Studies, Prospective Studies, Cerebrovascular Circulation, Aged, Aged, 80 and over, Middle Aged, Female, Male, Amyloid beta-Peptides