Stimulated release of the beta-amyloid protein of Alzheimer's disease by normal human platelets.

The circulatory system is a potential source of the beta-amyloid protein (A beta) of ageing and Alzheimer's disease (AD), platelets accounting for the bulk of A beta immunoreactivity detectable in blood. Evidence for the release of A beta by platelets, however, has not been reported. Platelets from normal donors were therefore stimulated with collagen to establish if A beta immunoreactive material is released on activation. For comparison, the release of the platelet monoamines, serotonin (5-HT) adrenaline (Adr) and noradrenaline (NA) was also measured. Like the monoamines, collagen-induced A beta release was concentration-dependent, maximal stimulated release exceeding basal efflux by 184%. Collagen EC50 values for A beta release were similar to those for Adr and NA (3.6 +/- 0.6, 3.4 +/- 0.6 and 3.3 +/- 0.2 microg/ml collagen, respectively) but not 5-HT (9.8 +/- 1.9 microg/ml). These data provide the first evidence that platelets release A beta immunoreactive material on stimulation and may indicate that A beta, Adr and NA reside in the same subcellular compartment.