beta-amyloid decreases detectable endothelial nitric oxide synthase in human erythrocytes: a role for membrane acetylcholinesterase

Until few years ago, many studies of Alzheimer's disease investigated the effects of this syndrome in the central nervous system. Only recently, the detection of amyloid beta peptide (A beta) in the blood has evidenced the necessity to extend studies on extraneuronal cells, particularly on erythrocytes. A beta is also present in brain capillaries, where it interacts with the erythrocytes, inducing several metabolic and functional alterations. Recently, functionally active endothelial type nitric oxide synthase (eNOS) was discovered in human erythrocytes. The goal of the present study was to evidence the effect of A beta on erythrocyte eNOS. We found that A beta following to 24-h exposure causes a decrease in the immune staining of erythrocyte eNOS. Concurrently, A beta alters erythrocyte cell morphology, decreases nitrites and nitrates levels, and affects membrane acetylcholinesterase activity. Propidium, an acetylcholinesterase inhibitor, was able to reverse the effects elicited by A beta. These events could contribute to the vascular alterations associated with Alzheimer's disease disease.