The overnight reduction of amyloid β 1-42 plasma levels is diminished by the extent of sleep fragmentation, sAPP-β, and APOE ε4 in psychiatrists on call.

Abstract

In mice there might be an association between sleep deprivation and amyloid β plasma levels. Hence, we examined whether amyloid plasma levels are associated with sleep duration or fragmentation in 17 psychiatrists on-call. Amyloid β (Aβ)42, Aβ40, and soluble amyloid precursor protein β (sAPP-β) plasma concentrations were measured at the beginning and end of 90 on-call nights, and analyzed using generalized linear models. In on-call nights, a 10.7% reduction of Aβ42 was revealed overnight. Every single short sleep interruption diminished this reduction by 5.4%, as well as every pg/mL of sAPP-β by 1.2%, each copy of APOE ε4 by 10.6%, and each year of professional experience by 3.0%. The extent of sleep fragmentation diminishes the physiological overnight reduction of Aβ42 but not Aβ40 plasma levels in the same direction as the enzyme for Aβ42 production, the genetic risk factor for Alzheimer's disease (AD), and on-call experience. Might on-call duty and sleep fragmentation in general alter the risk for AD?