Contrary, Davies et al. (1993 and 1997) showed that AD patients’ platelets activated by α-thrombin, compared to those of controls and to those of patients with other brain neurodegenerative diseases (the groups were not matched by age and gender), tended to abnormally hyperacidify, to accumulate unprocessed 120–130 kDa APP on their surface and to release less sAPP. The gene discussed is APP; the disease is Alzheimer disease.