EFFECTS OF PLASMA FROM PATIENTS AFFECTED BY MILD COGNITIVE IMPAIRMENT AND ALZHEIMER'S DISEASE ON CULTURED ENDOTHELIAL CELLS

被引:2
作者
Salvolini, E. [1 ]
Vignini, A. [2 ]
Nanetti, L. [2 ]
Luzzi, S. [3 ]
Provinciali, L. [3 ]
Di Primio, R. [1 ]
Mazzanti, L. [2 ]
机构
[1] Univ Politecn Marche, Dipartimento Sci Clin & Mol Istol, I-60126 Ancona, Italy
[2] Univ Politecn Marche, Dipartimento Sci Clin Specialist & Odontostomatol, I-60126 Ancona, Italy
[3] Univ Politecn Marche, Dipartimento Med Sperimentale & Clin, Clin Neurol, I-60126 Ancona, Italy
关键词
Alzheimer's disease; endothelial cells; nitric oxide; superoxide dismutase; Na+/K+-ATPase; membrane fluidity; TBARS; NITRIC-OXIDE; OXIDATIVE STRESS; DYSFUNCTION; DAMAGE; NA; K-ATPASE; MECHANISMS; DEMENTIA; DISORDER; LESIONS; ATPASE;
D O I
10.1177/1721727X1301100216
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:469 / 477
页数:9
相关论文
共 31 条
[1]  
Aliev G, 2002, BRAIN PATHOL, V12, P21
[2]   Modifications of platelet from Alzheimer disease patients: A possible relation between membrane properties and NO metabolites [J].
Arianna, Vignini ;
Laura, Nanetti ;
Cinzia, Moroni ;
Laura, Tanase ;
Marco, Bartolini ;
Simona, Luzzi ;
Leandro, Provinciali ;
Laura, Mazzanti .
NEUROBIOLOGY OF AGING, 2007, 28 (07) :987-994
[3]  
Baldeiras I, 2008, J ALZHEIMERS DIS, V15, P117
[4]   Human aortocoronary grafts and nitric oxide release: Relationship to pulsatile pressure [J].
Bilfinger, TV ;
Stefano, GB .
ANNALS OF THORACIC SURGERY, 2000, 69 (02) :480-485
[5]   Peripheral blood abnormalities in Alzheimer disease: Evidence for early endothelial dysfunction [J].
Borroni, B ;
Volpi, R ;
Martini, G ;
Del Bono, R ;
Archetti, S ;
Colciaghi, F ;
Akkawi, NM ;
Di Luca, M ;
Romanelli, G ;
Caimi, L ;
Padovani, A .
ALZHEIMER DISEASE & ASSOCIATED DISORDERS, 2002, 16 (03) :150-155
[6]   MORPHOLOGICAL CRITERIA FOR THE RECOGNITION OF ALZHEIMERS-DISEASE AND THE DISTRIBUTION PATTERN OF CORTICAL CHANGES RELATED TO THIS DISORDER [J].
BRAAK, H .
NEUROBIOLOGY OF AGING, 1994, 15 (03) :355-356
[7]  
Cester N, 1998, EUR J CLIN INVEST, V28, P989
[8]   Is Alzheimer's disease preceded by neurodegeneration or cerebral hypoperfusion? [J].
de la Torre, JC .
ANNALS OF NEUROLOGY, 2005, 57 (06) :783-784
[9]   Evidence that Alzheimer's disease is a microvascular disorder: the role of constitutive nitric oxide [J].
de la Torre, JC ;
Stefano, GB .
BRAIN RESEARCH REVIEWS, 2000, 34 (03) :119-136
[10]   Platelets as a peripheral district where to study pathogenetic mechanisms of Alzheimer disease: the case of amyloid precursor protein [J].
Di Luca, M ;
Colciaghi, F ;
Pastorino, L ;
Borroni, B ;
Padovani, A ;
Cattabeni, F .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2000, 405 (1-3) :277-283