Increased apoptosis in the platelets of patients with Alzheimer’s disease and amnestic mild cognitive impairment

• Increased apoptosis exist in the platelets of Alzheimer’s disease.
• Abnormal apoptosis may appear in the early of AD.
• The ratio between pro- and anti-apoptotic protein levels partially determines the susceptibility of platelet to a death signal.
• Platelet may be a good model to study apoptotic pathways of AD.

ObjectivesAlzheimer’s disease (AD), the most common cause of dementia, is a progressive, incurable neurodegenerative disorder. Platelet is a suitable source of human peripheral tissue to study pathological mechanisms occurring in the brain. The present study aims to investigate (1) whether abnormal apoptotic events besides involved in AD within the central neurologic system, could also occur at peripheral platelet level; (2) whether apoptosis at peripheral platelet level starts at the early stage of AD.Patients and methodsAmnestic mild cognitive impairment (MCI), AD, and age-matched healthy individuals were recruited, and each group had 50 person. In the present study, we investigate whether alterations of caspase family and Bcl2 family could be found in the platelets in Alzheimer’s disease (AD) and amnestic mild cognitive impairment (MCI) patients. The platelet levels of caspase protein and Bcl2 family were analyzed by western blot.ResultsThe results show that the platelet levels of caspase-3, caspase-9, Bad, and Bax significantly increased in AD and amnestic MCI. The increased apoptosis proteins levels in amnestic MCI were found between AD and normal controls. The anti-apoptosis protein Bcl2 increased in amnestic MCI, while decreased in AD.ConclusionWe suggest that increased apoptosis exist in the platelet and might mirror apoptosis within the brain. Abnormal apoptosis may appear in the early of AD, and the ratio between pro- and anti-apoptotic protein levels partially determines the susceptibility of platelet to a death signal. In conclusion, platelet may be a good model to study apoptotic pathways of AD.