Chemical-Driven Outflow of Dissociated Amyloid Burden from Brain to Blood

Amyloid-beta (A beta) deposition in the brain is a primary biomarker of Alzheimer's disease (AD) and A beta measurement for AD diagnosis mostly depends on brain imaging and cerebrospinal fluid analyses. Blood A beta can become a reliable surrogate biomarker if issues of low concentration for conventional laboratory instruments and uncertain correlation with brain A beta are solved. Here, brain-to-blood efflux of A beta is stimulated in AD transgenic mice by orally administrating a chemical that dissociates amyloid plaques and observing the subsequent increase of blood A beta concentration. 5XFAD transgenic and wild-type mice of varying ages and genders are prepared, and blood samples of each mouse are collected six times for 12 weeks; three weeks of no treatment and additional nine weeks of daily oral administration, ad libitum, of A beta plaque-dissociating chemical agent. By the dissociation of A beta aggregates, the altered levels of plasma A beta distinguish between transgenic and wild-type mice, displaying potential as an amyloid burden marker of AD brains.

Automated summary

In this study, brain-to-blood efflux of Aβ in AD transgenic mice was stimulated by orally administrating a chemical, and the altered levels of blood Aβ showed potential as an amyloid burden marker of AD brains.