[Platelet function in patients with Alzheimer disease: analysis of 40 cases]

To investigate the platelet aggregation in Alzheimer disease (AD) patients and the influence of platelet-derived nitric oxide (NO) on such aggregation.

Peripheral blood samples were collected from 40 mild and moderate AD patients, 20 males and 20 females, aged (72 +/- 8), and 42 healthy controls, 13 males and 29 females, aged (69 +/- 4). Turbidimetry was used to measure the platelet aggregation, colorimetry was used to detect the concentration of nitric oxide, and the activity levels of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in platelets were examined with nitric oxide synthase assay kit The correlation among these variables was analyzed.

The platelet aggregation rate of the AD patients was (58% +/- 12%), significantly higher than that of the healthy controls (53% +/- 9%, P < 0.05). The NO concentration of the AD patients was (0. 743 +/- 0.164) nmol x 10(8) pt(-1), significantly lower than that of the healthy controls [(0.874 +/- 0.378) nmol x 10(8) pt(-1), P < 0.05]. In the AD patients, the platelet aggregation rate was negatively correlated with the NO concentration (r = -0.358, P < 0.05). The eNOS activity level in platelet of the AD patients was (0.040 +/- 0.016) nmol x 10(8) pt(-1) x min(-1), significantly lower than that of the controls [(0.050 +/- 0.023) nmol x 10(8) pt(-1) x min(-1), P < 0.05]. The iNOS activity level of the AD patients was (0.037 +/- 0.016) nmol x 10(8) pt(-1) x min(-1), not significantly different from that of the controls [(0.043 +/- 0.021) nmol x 10(8) pt(-1) x min(-1), P > 0.05]. In the AD group, the platelet-derived nitric oxide level was positively correlated with the activity level of eNOS (r = 0.326, P < 0.05). There were no significant differences in platelet aggregation, NO concentration, and eNOS, iNOS, and total NOS activity levels between the mild and moderate AD patients.

The decline of eNOS activity that reduces the NO concentration of platelet may increase the platelet aggregation in the AD patients, since NO can inhibit platelet aggregation. Anti-platelet drug and NO promoting drug may be used to treat AD.