Effects of Plasma from Patients Affected by Mild Cognitive Impairment and Alzheimer's Disease on Cultured Endothelial Cells. (May 2013)

• Record Type: Journal Article
• Authors: Salvolini, E.; Vignini, A.; Nanetti, L.; Luzzi, S.; Provinciali, L.; Di Primio, R.; Mazzanti, L.
• Is Part Of: European journal of inflammation. Volume 11:Number 2(2013)
• Page Start: 469
• Page End: 477
• Publication Date: 2013-05
• Subjects: Alzheimer's disease -- endothelial cells -- nitric oxide -- superoxide dismutase -- Na+/K+-ATPase -- membrane fluidity -- TBARS; Inflammation -- Periodicals; Anti-Inflammatory Agents -- therapeutic use -- Periodicals; Immunotherapy -- Periodicals; Inflammation -- Periodicals; Anti-inflammatory agents -- Periodicals; Immunotherapy -- Periodicals; Anti-inflammatory agents; Immunotherapy; Inflammation; Periodicals; 616.0473
• DOI: 10.1177/1721727X1301100216
• Languages: English
• ISSNs: 1721-727X

Abstract

There is accumulating evidence that Alzheimer's disease (AD) can have vascular contribution. In particular, endothelial dysfunction may impair nitric oxide (NO) production and cause cerebral hypoperfusion. Blood flow impairment can be provoked also by an increased production of reactive oxygen species (ROS). The present study was performed in order to investigate the effect of plasma from subjects affected by AD and mild cognitive impairment (MCI) on human aortic endothelial cells (HAECs) in vitro, since endothelial dysfunction has been suggested to be an early event in patients affected by AD. Plasma samples were obtained from 27 AD patients, 15 MCI subjects, and 19 age-and sex-matched healthy subjects. After a short incubation period the following parameters were evaluated: NO release, superoxide dismutase (SOD) and Na + /K + -ATPase activities, membrane fluidity, and thiobarbituric acid-reactive substance (TBARS) production. Exposure to MCI plasma provoked a decrease in NO release, more pronounced in the presence of AD plasma. Our data on SOD and Na + /K + -ATPase activities showed a similar trend, since the lowest values were recorded after incubation with AD plasma. Endothelial membrane fluidity was deeply affected by the exposure to MCI plasma, and even more following incubation with AD plasma. Finally, enhanced TBARS production after incubation with MCI and AD plasma was observed. In conclusion, our results showed that MCI and AD plasma affects endothelial cells, thus highlighting the need for early treatment aimed at protecting the endothelium.