PLATELET PHOSPHATIDYLINOSITOL KINASE-ACTIVITY IS NOT ALTERED IN ALZHEIMER-DISEASE

We previously reported a specific decline in phosphatidylinositol (PI) kinase activity in the neocortex of patients with Alzheimer disease ( AD) as compared to controls, whereas phosphatidylinositol phosphate (P IP) kinase activity appeared not to be affected (jolles et al., 1992). In search of a possible systemic effect of AD, in the present study w e investigated phosphoinositide kinase activity in platelets from pati ents with AD and from control subjects. The study was based on the not ion that disease-specific abnormalities in the brain could be reflecte d in blood platelets. PI kinase activity was studied in platelet homog enates and in a salt-solubilized protein fraction of platelets, becaus e of the difference in subcellular localization of the different types of PI kinases. In addition, NADH cytochrome-C reductase was measured in platelet homogenates as a marker for the endoplasmic reticulum, to detect a possible proliferation of the endoplasmic reticulum. AD patie nts and normal elderly controls showed no difference in PI kinase acti vity in either enzyme fraction. Furthermore, NADH cytochrome-C reducta se activity and the protein/phospholipid ratio per 10(6) platelets wer e the same for AD patients and controls. This was taken as an indicati on that platelets in AD patients do not show proliferation of intracel lular membranes.