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新研究揭示了糖尿病可能导致阿尔茨海默病的原因 精选

已有 6302 次阅读 2024-8-24 15:11 |个人分类:新观察|系统分类:博客资讯

新研究揭示了糖尿病可能导致阿尔茨海默病的原因

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Fig. 1 Research from Umeå University shows that type 2 diabetes impedes the elimination of Alzheimer’s-related proteins, suggesting a higher cognitive risk, highlighting the importance of diabetes management.

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Fig. 2 Professor Olov Rolandsson, Department of Public Health and Clinical Medicine, Umeå University. Credit: Mattias Pettersson

据瑞典于默奥大学Umeå University, Umeå, Sweden2024822日提供的消息,该校研究人员领导、其他来自瑞典、英国、中国、美国、法国等机构研究人员参与的一项新研究,揭示了糖尿病可能导致阿尔茨海默病的原因(New Research Reveals Why Diabetes Could Lead to Alzheimer’s Disease)。研究表明,2型糖尿病可能会损害阿尔茨海默氏症相关蛋白(Alzheimer’s-related proteins)的消除,这提示了通过控制血糖水平来减轻认知风险的潜在策略。

2型糖尿病患者患阿尔茨海默病和其他认知问题的风险更高。瑞典于默奥大学等多国机构参与的最近一项研究表明,这种风险的增加可能是由于2型糖尿病患者难以清除一种可能与该疾病有关的蛋白质。相关研究结果于2024528日已经在《阿尔茨海默病杂志》(Journal of Alzheimer's Disease网站在线发表——Olov RolandssonAndreas TorneviPär StenebergHelena EdlundTommy OlssonUlf AndreassonHenrik ZetterbergKaj Blennow. Acute Hyperglycemia Induced by Hyperglycemic Clamp Affects Plasma Amyloid-β in Type 2 Diabetes. Journal of Alzheimer's Disease, 2024, 99(3): 1033-1046. DOI: 10.3233/JAD-230628. Published: 28 May 2024. https://content.iospress.com/articles/journal-of-alzheimers-disease/jad230628

参与此项研究的除了来自瑞典于默奥大学的研究人员,还有来自瑞典哥德堡大学(University of Gothenburg, Gothenburg, Sweden)、瑞典默恩达尔的萨尔格林斯卡大学医院(Sahlgrenska University Hospital, Mölndal, Sweden);英国伦敦大学学院神经学研究所(UCL Institute of Neurology, London, UK)、英国伦敦大学学院痴呆症研究所(Dementia Research Institute at UCL, London, UK);中国香港神经退行性疾病中心(Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China)、中国合肥中国科学技术大学及其第一附属医院(University of Science and Technology of China and First Affiliated Hospital of USTC, Hefei, China);美国威斯康辛大学麦迪逊分校医学与公共卫生学院(University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA)、法国巴黎的索邦大学(Sorbonne University, Paris, France)的研究人员。

于默奥大学公共卫生和临床医学、家庭医学系(Department of Public Health and Clinical Medicine, Family Medicine, Umeå University, Umeå, Sweden)资深教授、该研究的负责人和上述研究论文的第一作者Olov Rolandsson说:“这一结果可能对进一步研究可能的治疗方法很重要,以抵消2型糖尿病患者患阿尔茨海默氏症的风险。”

研究人员研究的物质是两种所谓的β-淀粉样蛋白(beta-amyloids),它们是阿尔茨海默病患者大脑中发现的斑块的最重要成分之一。

β-淀粉样蛋白的研究结果(Study Findings on Beta-Amyloids

研究人员测量了2型糖尿病试验组和健康对照组血液中β-淀粉样蛋白Aβ1-40Aβ1-42的浓度,以及一种分解β-淀粉样蛋白的酶的浓度。两组均输注葡萄糖4 h,引起急性高血糖(acute hyperglycemia),即高血糖水平。输注葡萄糖4 h后,对受试者重复取样。

糖溶液输注后,两组的数值相近。很快,在对照组中,β-淀粉样蛋白的值急剧下降,而淀粉样蛋白降解酶的值上升。在2型糖尿病患者中,没有变化,即β-淀粉样蛋白的水平没有下降,分解淀粉样蛋白的酶也没有增加。

结果表明,2型糖尿病患者的身体不像健康人那样有能力处理β-淀粉样蛋白,这可能会增加β-淀粉样蛋白储存在大脑中的风险,从而导致阿尔茨海默氏症等认知疾病。

“需要更多的研究来证实这项有限研究的结果。希望从长远来看,它也能带来新的治疗方法。但研究结果强调了尽可能预防2型糖尿病的重要性,患有2型糖尿病的人应该避免高血糖发作,”Olov Rolandsson说。

这项研究是在102型糖尿病患者和11名非糖尿病患者作为对照组进行的。参与者的年龄为66~72岁。

上述介绍,仅供参考。欲了解更多信息,敬请注意浏览原文或者相关报道

Abstract

Background: Individuals with type 2 diabetes (T2D) have an increased risk of cognitive symptoms and Alzheimer's disease (AD). Mis-metabolism with aggregation of amyloid-β peptides (Aβ) play a key role in AD pathophysiology. Therefore, human studies on Aβ metabolism and T2D are warranted.

Objective: The objective of this study was to examine whether acute hyperglycemia affects plasma Aβ1-40 and Aβ1-42 concentrations in individuals with T2D and matched controls.

Methods: Ten participants with T2D and 11 controls (median age, 69 years; range, 66-72 years) underwent hyperglycemic clamp and placebo clamp (saline infusion) in a randomized order, each lasting 4 hours. Aβ1-40, Aβ1-42, and insulin-degrading enzyme (IDE) plasma concentrations were measured in blood samples taken at 0 and 4 hours of each clamp. Linear mixed-effect regression models were used to evaluate the 4-hour changes in Aβ1-40 and Aβ1-42 concentrations, adjusting for body mass index, estimated glomerular filtration rate, and 4-hour change in insulin concentration.

Results: At baseline, Aβ1-40 and Aβ1-42 concentrations did not differ between the two groups. During the hyperglycemic clamp, Aβ decreased in the control group, compared to the placebo clamp (Aβ1-40: p = 0.034, Aβ1-42: p = 0.020), IDE increased (p = 0.016) during the hyperglycemic clamp, whereas no significant changes in either Aβ or IDE was noted in the T2D group.

Conclusions: Clamp-induced hyperglycemia was associated with increased IDE levels and enhanced Aβ40 and Aβ42 clearance in controls, but not in individuals with T2D. We hypothesize that insulin-degrading enzyme was inhibited during hyperglycemic conditions in people with T2D.



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