["Knowledge concerning the neurobiological importance of platelets in Alzheimer's disease (AD) is sparse. P-selectin, which is located together with β-amyloid precursor proteins in platelet α-granules, is also found in endothelial cells. Upon activation, P-selectin is relocated to cell surfaces where it acts as a receptor. Subsequently, the protein is cleaved from the membrane, to then be circulated. We investigated P-selectin behavior in AD dementia.", 'We recruited 23 persons diagnosed moderate AD and 17 healthy elders without obvious memory problems. Circulating P-selectin was analyzed using an ELISA technique and flow cytometry was used to measure surface-bound P-selectin. The latter measure was carried out without provocation (platelet activity) and after in vitro agonist stimulation (platelet reactivity). A thrombin-receptor activating peptide (TRAP-6) (74 μmol/L)) was used as a platelet agonist.', 'Soluble P-selectin was augmented in AD (p = 0.019) but platelet membrane-attached P-selectin did not differ from controls. AD diagnosis was associated with less surface-bound P-selectin after provocation. Significant results were obtained when 74 μmol/L TRAP-6 was used as a platelet agonist (p = 0.0008).'] Is p-selectin paradox and dementia of the Alzheimer type : circulating P-selectin increased but platelet-bound P-selectin after agonist provocation is compromised?