| First Author | Lee D | Year | 2022 |
| Journal | Adv Sci (Weinh) | Volume | 9 |
| Issue | 12 | Pages | e2104542 |
| PubMed ID | 35106958 | Mgi Jnum | J:351777 |
| Mgi Id | MGI:7664290 | Doi | 10.1002/advs.202104542 |
| Citation | Lee D, et al. (2022) Chemical-Driven Outflow of Dissociated Amyloid Burden from Brain to Blood. Adv Sci (Weinh) 9(12):e2104542 |
| abstractText | Amyloid-beta (Abeta) deposition in the brain is a primary biomarker of Alzheimer's disease (AD) and Abeta measurement for AD diagnosis mostly depends on brain imaging and cerebrospinal fluid analyses. Blood Abeta can become a reliable surrogate biomarker if issues of low concentration for conventional laboratory instruments and uncertain correlation with brain Abeta are solved. Here, brain-to-blood efflux of Abeta is stimulated in AD transgenic mice by orally administrating a chemical that dissociates amyloid plaques and observing the subsequent increase of blood Abeta 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 Abeta plaque-dissociating chemical agent. By the dissociation of Abeta aggregates, the altered levels of plasma Abeta distinguish between transgenic and wild-type mice, displaying potential as an amyloid burden marker of AD brains. |
