Abstract
Amyloid β protein deposition in cerebral vessels, a characteristic of Alzheimer's disease, is a risk factor for intracerebral hemorrhage. Amyloid β protein directly modulates human platelet function; however, the exact mechanism of action is unclear. Therefore, we investigated the effects of amyloid β protein on human platelet activation using an aggregometer with laser scattering. Amyloid β protein decreased platelet aggregation induced by thrombin receptor-activating protein, but not by collagen and ADP. Amyloid β protein also suppressed platelet aggregation induced by SCP0237 and A3227. Platelet-derived growth factor-AB secretion and phosphorylated-heat shock protein 27 release by thrombin receptor-activating protein were inhibited by amyloid β protein. Additionally, thrombin receptor-activating protein-induced phosphorylation of JNK and p38 MAP kinase was reduced by amyloid β protein. Collectively, our results strongly suggest that amyloid β protein negatively regulates protease-activated receptor-elicited human platelet activation. These findings may indicate a cause of intracerebral hemorrhage due to amyloid β protein.
Highlights
Amyloid β protein (Aβ) is the main product derived from amyloid precursor protein (APP) by sequential enzymatic actions
The results of the present study strongly suggest that Aβ negatively regulates protease-activated receptor (PAR)-elicited human platelet activation
The results strongly suggest that Aβ negatively regulates PAR-elicited human platelet activation, and may be one of the causes of intracerebral hemorrhage due to cerebral amyloid angiopathy (CAA)
Summary
Amyloid β protein (Aβ) is the main product derived from amyloid precursor protein (APP) by sequential enzymatic actions. Deposition of Aβ in the brain parenchyma or cerebral vessels is a primary morphological feature of Alzheimer’s disease (AD). Abnormal accumulation of Aβ in the cerebral vessels is known as cerebral amyloid angiopathy (CAA), which is considered a risk factor for intracerebral hemorrhage, in the elderly. Amyloid β protein (Aβ) is the main product derived from amyloid precursor protein (APP) [1]. Abnormal accumulation of Aβ due to the failure of clearance of amyloid occurs at the cerebral vessels, leading to cerebral amyloid angiopathy (CAA) [6]. Since CAA is reportedly observed in > 70% of individuals with AD, CAA is recognized as a feature of AD, and is considered as a contributor to vascular cognitive decline [9,10,11]. It has been shown that biochemical changes in patients with AD occur even in blood cells [12]
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