Plasma β amyloid and impaired CO2-induced cerebral vasomotor reactivity

van Dijk, Ewoud J.; Prins, Niels D.; Hofman, Albert; van Duijn, Cornelia M.; Koudstaal, Peter J.; Breteler, Monique M.B.

doi:10.1016/j.neurobiolaging.2006.03.011

« Previous Next »Neurobiology of Aging
Volume 28, Issue 5 , Pages 707-712, May 2007

Plasma β amyloid and impaired CO₂-induced cerebral vasomotor reactivity

Ewoud J. van Dijk
- Department of Epidemiology and Biostatistics, Erasmus MC, Erasmus University Medical Center, PO Box 1738, 3000 Rotterdam, The Netherlands
- Department of Neurology, Erasmus MC, Erasmus University Medical Center, Rotterdam, The Netherlands
Niels D. Prins
- Department of Epidemiology and Biostatistics, Erasmus MC, Erasmus University Medical Center, PO Box 1738, 3000 Rotterdam, The Netherlands
- Department of Neurology, Erasmus MC, Erasmus University Medical Center, Rotterdam, The Netherlands
Albert Hofman
- Department of Epidemiology and Biostatistics, Erasmus MC, Erasmus University Medical Center, PO Box 1738, 3000 Rotterdam, The Netherlands
Cornelia M. van Duijn
- Department of Epidemiology and Biostatistics, Erasmus MC, Erasmus University Medical Center, PO Box 1738, 3000 Rotterdam, The Netherlands
Peter J. Koudstaal
- Department of Neurology, Erasmus MC, Erasmus University Medical Center, Rotterdam, The Netherlands
Monique M.B. Breteler
- Department of Epidemiology and Biostatistics, Erasmus MC, Erasmus University Medical Center, PO Box 1738, 3000 Rotterdam, The Netherlands
- Corresponding author. Tel.: +31 10 4087489; fax: +31 10 4089382.

Received 31 August 2005; received in revised form 8 March 2006; accepted 31 March 2006. published online 24 May 2006.

Abstract

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 Aβ_1–40 and Aβ_1–42 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 Aβ_1–40, and 1.36 (95%CI 1.09;1.70) per standard deviation increase in Aβ_1–42). Such an association was not present for Aβ assessed concurrently with the TCD measurement. Persons whose plasma Aβ_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 Aβ levels representing vascular Aβ deposits years later resulting in impaired CO₂-induced vasomotor reactivity.