Colocalisation of plasma derived apo B lipoproteins with cerebral proteoglycans in a transgenic-amyloid model of Alzheimer's disease

Alzheimer's disease (AD) is characterized by cerebral proteinaceous deposits comprised of amyloid beta (A beta). Evidence suggests that enhanced blood-to-brain delivery of A beta occurs when plasma concentration is increased, exacerbating amyloidosis. In blood, significant A beta is associated with apolipoprotein (apo) B lipoproteins. In this study, immunofluorescent microscopy was utilised to explore if there is an association between apo B lipoproteins and proteoglycan expression within A beta-rich plaques in transgenic-amyloid mice. Focal accumulation of apo B was found with A beta-plaque in APP/PS1 mice. There was enrichment in the proteoglycans, agrin, perlecan, biglycan and decorin within the core of dense A beta-plaque. Perlecan, biglycan and decorin were positively associated with apo B lipoprotein abundance within amyloid plaque consistent with a cause-for-retention effect. These findings show that proteoglycans are an integral component of A beta deposits in APP/PS1 mice. This study suggests that some proteoglycans contribute to A beta retention, whilst other proteoglycans have different functions in the aetiology of AD. (C) 2011 Elsevier Ireland Ltd. All rights reserved.