PDF(Pubmed)
Abstract：
Amylin is a systemic neuroendocrine hormone co-expressed and co-secreted with insulin by pancreatic β-cells. In persons with thype-2 diabetes, amylin forms pancreatic amyloid triggering inflammasome and interleukin-1β signaling and inducing β-cell apoptosis. Here, we summarize recent progress in understanding the potential link between amyloid-forming pancreatic amylin and Alzheimer\'s disease (AD). Clinical data describing amylin pathology in AD alongside mechanistic studies in animals are reviewed. Data from multiple research teams indicate higher amylin concentrations are associated with increased frequency of cognitive impairment and amylin co-aggregates with β-amyloid in AD-type dementia. Evidence from rodent models further suggests cerebrovascular amylin accumulation as a causative factor underlying neurological deficits. Analysis of relevant literature suggests that modulating the amylin-interleukin-1β pathway may provide an approach for counteracting neuroinflammation in AD.
摘要：
胰淀素是由胰腺β细胞与胰岛素共表达和共分泌的全身性神经内分泌激素。在2型糖尿病患者中，胰淀素形成胰腺淀粉样蛋白，触发炎症小体和白细胞介素-1β信号并诱导β细胞凋亡。这里,我们总结了淀粉样蛋白形成胰腺胰淀素与阿尔茨海默病（AD）之间潜在联系的最新进展。回顾了描述AD中胰淀素病理学以及动物机理研究的临床数据。来自多个研究小组的数据表明，在AD型痴呆中，较高的胰淀素浓度与认知障碍和胰淀素与β-淀粉样蛋白共聚集的频率增加有关。来自啮齿动物模型的证据进一步表明，脑血管胰淀素的积累是神经系统缺陷的致病因素。对相关文献的分析表明，调节胰淀素-白介素-1β途径可能为抵抗AD中的神经炎症提供了一种方法。
