Abstract:
Many studies indicate that there is a (mainly dormant) microbial component in the
progressive development of Alzheimer-type dementias (ADs); and that in the case
of Gram-negative organisms, a chief culprit might be the shedding of the highly
inflammagenic lipopolysaccharide (LPS) from their cell walls. We have recently shown
that a highly sensitive assay for the presence of free LPS [added to platelet poor plasma
(PPP)] lies in its ability (in healthy individuals) to induce blood to clot into an amyloid
form. This may be observed in a SEM or in a confocal microscope when suitable
amyloid stains (such as thioflavin T) are added. This process could be inhibited by human
lipopolysaccharide-binding protein (LBP). In the current paper, we show using scanning
electron microscopy and confocal microscopy with amyloid markers, that PPP taken
from individuals with AD exhibits considerable amyloid structure when clotting is initiated
with thrombin but without added LPS. Furthermore, we could show that this amyloid
structure may be reversed by the addition of very small amounts of LBP. This provides
further evidence for a role of microbes and their inflammagenic cell wall products and
that these products may be involved in pathological clotting in individuals with AD.
