Blood-borne factors inhibit Alzheimer's β-amyloid fibril formation in vitro

Soluble amyloid β-protein (Aβ) does not aggregate to β-amyloid fibrils (fAβ) in the brain of normal humans. We recently found that the cerebrospinal fluid (CSF) from non-Alzheimer's disease (AD) subjects inhibited the formation of fAβ(1–40) and fAβ(1–42) more strongly than that from AD subjects, although the CSF obtained from both groups inhibited the fAβs formation in vitro. Here, we examined the influence of plasma obtained from AD, non-AD and healthy control (CTL) subjects on the formation of fAβ(1–40) and fAβ(1–42) in vitro. Although the plasma obtained from all groups inhibited the formation of fAβ(1–40) and fAβ(1–42), the plasma from non-AD and CTL subjects inhibited the formation of fAβs more strongly than that from AD subjects. These results indicate that the plasma as well as CSF in AD would provide a molecular environment favorable for fAβ formation, suggesting a decrease of specific inhibitory factors and/or increase of specific accelerating factors.