阿尔茨海默病和青光眼患者血小板生成的淀粉样β肽。
Platelet-generated amyloid beta peptides in Alzheimer's disease and glaucoma.
机构信息
School of Medicine, Universidad Central del Caribe (UCC), PR, USA.
出版信息
Histol Histopathol. 2019 Aug;34(8):843-856. doi: 10.14670/HH-18-111. Epub 2019 Apr 4.
Abstract
Amyloid beta (Aβ) peptides have been implicated in both Alzheimer's disease (AD) and glaucoma and have been shown to be the key etiological factor in these dangerous health complications. On the other hand, it is well known that Aβ peptide can be generated from its precursor protein and massively released from the blood to nearby tissue upon the activation of platelets due to their involvement in innate immunity and inflammation processes. Here we review evidence about the development of AD and glaucoma neuronal damage showing their dependence on platelet count and activation. The correlation between the effect on platelet count and the effectiveness of anti-AD and anti-glaucoma therapies suggest that platelets may be an important player in these diseases.
摘要
淀粉样β（Aβ）肽与阿尔茨海默病（AD）和青光眼均有关联，并且已被证明是这些危险健康并发症的关键病因。另一方面，众所周知，由于血小板参与先天免疫和炎症过程，当血小板被激活时，Aβ肽可以从其前体蛋白产生，并大量从血液释放到附近组织。在这里，我们回顾了有关 AD 和青光眼神经元损伤发展的证据，表明它们依赖于血小板计数和激活。血小板计数的影响与抗 AD 和抗青光眼治疗效果之间的相关性表明，血小板可能是这些疾病的重要参与者。
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