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International Journal of Alzheimer’s Disease
Volume 2014 (2014), Article ID 191863, 7 pages
Research Article

The Role of the Blood-Brain Barrier in the Pathogenesis of Senile Plaques in Alzheimer’s Disease

1Department of Pathology & Molecular Medicine (Neuropathology), Hamilton Health Sciences, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4L8
2Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, 500 Glenridge Avenue, STH 315, St. Catharines, ON, Canada L2S 3A1

Received 19 June 2014; Revised 3 September 2014; Accepted 8 September 2014; Published 18 September 2014

Academic Editor: Francesco Panza

Copyright © 2014 J. Provias and B. Jeynes. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The accumulation of beta-amyloid [Aβ] within senile plaques [SP] is characteristic of these lesions in Alzheimer’s disease. The accumulation of Aβ42, in particular, in the superior temporal [ST] cortex may result from an inability of the blood brain barrier (BBB) to regulate the trans-endothelial transport and clearance of the amyloid. Lipoprotein receptor-related protein [LRP] and P-glycoprotein [P-gp] facilitate the efflux of Aβ out of the brain, whereas receptor for advanced glycation end products [RAGE] facilitates Aβ influx. Additionally, vascular endothelial growth factor [VEGF] and endothelial nitric oxide synthase [eNOS] may influence the trans-BBB transport of Aβ. In this study we examined ST samples and compared SP burden of all types with the capillary expression of LRP, p-gp, RAGE, VEGF, and e-NOS in samples from 15 control and 15 Alzheimer brains. LRP, P-gp, RAGE, VEGF, and eNOS positive capillaries and Aβ42 plaques were quantified and statistical analysis of the nonparametric data was performed using the Mann-Whitney and Kruskal-Wallis tests. In the Alzheimer condition P-gp, VEGF, and eNOS positive capillaries were negatively correlated with SP burden, but LRP and RAGE were positively correlated with SP burden. These results indicate altered BBB function in the pathogenesis of SPs in Alzheimer brains.