| First Author | Lam V | Year | 2011 |
| Journal | Neurosci Lett | Volume | 492 |
| Issue | 3 | Pages | 160-4 |
| PubMed ID | 21310214 | Mgi Jnum | J:170853 |
| Mgi Id | MGI:4947482 | Doi | 10.1016/j.neulet.2011.02.001 |
| Citation | Lam V, et al. (2011) Colocalisation of plasma derived apo B lipoproteins with cerebral proteoglycans in a transgenic-amyloid model of Alzheimer's disease. Neurosci Lett 492(3):160-4 |
| abstractText | Alzheimer's disease (AD) is characterized by cerebral proteinaceous deposits comprised of amyloid beta (Abeta). Evidence suggests that enhanced blood-to-brain delivery of Abeta occurs when plasma concentration is increased, exacerbating amyloidosis. In blood, significant Abeta 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 Abeta-rich plaques in transgenic-amyloid mice. Focal accumulation of apo B was found with Abeta-plaque in APP/PS1 mice. There was enrichment in the proteoglycans, agrin, perlecan, biglycan and decorin within the core of dense Abeta-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 Abeta deposits in APP/PS1 mice. This study suggests that some proteoglycans contribute to Abeta retention, whilst other proteoglycans have different functions in the aetiology of AD. |
