Immunohistochemical study of semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 in the hippocampal vasculature: Pathological synergy of Alzheimer's disease and diabetes mellitus
Article first published online: 20 JUN 2012
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Neuroscience Research
Volume 90, Issue 10, pages 1989–1996, October 2012
How to Cite
Valente, T., Gella, A., Solé, M., Durany, N. and Unzeta, M. (2012), Immunohistochemical study of semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 in the hippocampal vasculature: Pathological synergy of Alzheimer's disease and diabetes mellitus. J. Neurosci. Res., 90: 1989–1996. doi: 10.1002/jnr.23092
T. Valente and A. Gella contributed equally to this work.
- Issue published online: 8 AUG 2012
- Article first published online: 20 JUN 2012
- Manuscript Accepted: 20 APR 2012
- Manuscript Revised: 17 APR 2012
- Manuscript Received: 27 DEC 2011
- Spanish Ministerio de Ciencia y Tecnologia. Grant Number: SAF 2006-08764-C02-02
- Ministerio de Industria, programa INGENIO 2010, proyecto CENIT. Grant Number: MET-DEV-FUN 2006-2009
- Spanish Ministerio de Ciencia e Innovación
- Alzheimer's disease;
- diabetes mellitus;
- advanced glycation end products;
- cerebral blood vessels;
Semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 (SSAO/VAP-1) is involved in vascular endothelial damage as well as in the vascular degeneration underlying diabetes mellitus and Alzheimer's disease (AD). Recent evidence suggests that classic pathological features of AD are more pronounced in diabetic mellitus patients. To investigate the expression and distribution of SSAO/VAP-1 in the two pathologies, we have performed an immunohistochemical study in human hippocampal vessels of AD, AD with diabetic mellitus (ADD), diabetic mellitus (DM), and nondemented (ND) patients. The present results demonstrate major vessel accumulation of both SSAO/VAP-1 and amyloid-β immunolabeling intensity in ADD compared with AD patients. Interestingly, nearly damaged vessels with high levels of SSAO/VAP-1 also showed increased oxidative damage markers (AGE, RAGE, and SOD-1) and glial activation (GFAP and HLA). Overall, this work suggests that high vascular SSAO/VAP-1 levels in human hippocampus may contribute to vascular degeneration, which can explain the severe progression in patients with both pathologies. © 2012 Wiley Periodicals, Inc.