Type 2 DM is a risk factor for dementia, including Alzheimer's disease (AD), and is associated with brain atrophy. Amyloid β protein (Aβ) deposition in the brain parenchyma is implicated in the neurodegeneration that occurs in AD. Platelets, known as abundant storage of Aβ, are recognized to play important roles in the onset and progression of AD. We recently showed that Aβ negatively regulates platelet activation induced by thrombin receptor-activating protein (TRAP) in healthy people. In the present study, we investigated the effects of Aβ on the TRAP-stimulated platelet activation in DM patients, and the relationship between the individual responsiveness to Aβ and quantitative findings of MRI, the volume of white matter hyperintensity (WMH)/intracranial volume (IC) and the volume of parenchyma (PAR)/IC. In some DM patients, Aβ reduced platelet aggregation induced by TRAP, while in others it was unchanged or rather enhanced. The TRAP-induced levels of phosphorylated-Akt and phosphorylated-HSP27, the levels of PDGF-AB and the released phosphorylated-HSP27 correlated with the degree of platelet aggregability. The individual levels of not WMH/IC but PAR/IC was correlated with those of TRAP-stimulated PDGF-AB release. Collectively, our results suggest that the reactivity of TRAP-stimulated platelet activation to Aβ differs in DM patients from healthy people. The anti-suppressive feature of platelet activation to Aβ might be protective for brain atrophy in DM patients.
Keywords: Amyloid β protein; brain atrophy; diabetes mellitus; platelet; platelet-derived growth factor; thrombin receptor-activating protein.