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Parenchymal accumulation of amyloid-beta (A beta) is a hallmark pathological feature of Alzheimer's disease. An emerging hypothesis is that blood-to-brain delivery of A beta may increase with compromised blood-brain barrier integrity. In plasma, substantial A beta is associated with triglyceride-rich lipoproteins (TRLs) secreted by the liver and intestine. Utilizing apolipoprotein B as an exclusive marker of hepatic and intestinal TRLs, here we show utilizing an highly sensitive 3-dimensional immuno-microscopy imaging technique, that in APP/PS1 amyloid transgenic mice, concomitant with substantially increased plasma A beta, there is a significant colocalization of apolipoprotein B with cerebral amyloid plaque. The findings are consistent with the possibility that circulating lipoprotein-A beta contributes to cerebral amyloidosis.

Original publication

DOI

10.1007/s00418-009-0567-3

Type

Journal article

Journal

Histochem Cell Biol

Publication Date

05/2009

Volume

131

Pages

661 - 666

Keywords

Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Apolipoproteins B, Brain, Humans, Mice, Mice, Transgenic, Microscopy, Fluorescence, Oligopeptides, Plaque, Amyloid, Protease Nexins, Receptors, Cell Surface