使用降糖药物胰高血糖素样肽1受体激动剂治疗阿尔茨海默病的新证据

Ides M Colin, Lidia W Szczepanski, Anne-Catherine Gérard, Jose-Antonio Elosegi
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引用次数: 2

摘要

从流行病学和病理生理学的角度来看,阿尔茨海默病(AD)和2型糖尿病(T2DM)应被视为“姐妹”疾病。T2DM显著增加AD发生的风险,且神经元退行性变本身的机制通过多种途径恶化外周糖代谢。这两种疾病之间的病理生理联系,特别是导致神经元变性的脑胰岛素抵抗,是如此紧密,以至于阿尔茨海默病有时被称为“3型糖尿病”。尽管阿尔茨海默病治疗前沿的最新消息令人鼓舞,但没有任何治疗方法被证明可以永久阻止疾病进展。治疗充其量只能减缓病情的发展;在最坏的情况下,它们是无效的,或者会引起令人担忧的副作用,从而阻止它们的大规模使用。因此,通过预防或治疗措施优化代谢环境也可以减缓AD特征的大脑变性,这似乎是合乎逻辑的。在不同类型的降糖药物中,广泛用于治疗T2DM的胰高血糖素样肽1受体激动剂(glucagon-like peptide 1 receptor agonists)被证明可以减缓甚至预防神经元变性。来自动物、临床前、临床II期、队列和大型心血管结局研究的数据令人鼓舞。当然,正在进行的随机临床III期研究将对验证这一假设至关重要。因此,这一次,有希望减缓与糖尿病相关的神经退行性过程,这一希望是本综述的重点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Emerging Evidence for the Use of Antidiabetic Drugs, Glucagon-like Peptide 1 Receptor Agonists, for the Treatment of Alzheimer's Disease.

Emerging Evidence for the Use of Antidiabetic Drugs, Glucagon-like Peptide 1 Receptor Agonists, for the Treatment of Alzheimer's Disease.

Emerging Evidence for the Use of Antidiabetic Drugs, Glucagon-like Peptide 1 Receptor Agonists, for the Treatment of Alzheimer's Disease.

Emerging Evidence for the Use of Antidiabetic Drugs, Glucagon-like Peptide 1 Receptor Agonists, for the Treatment of Alzheimer's Disease.

From an epidemiological and pathophysiological point of view, Alzheimer's disease (AD) and type 2 diabetes (T2DM) should be considered 'sister' diseases. T2DM significantly increases the risk of developing AD, and the mechanisms of neuronal degeneration themselves worsen peripheral glucose metabolism in multiple ways. The pathophysiological links between the two diseases, particularly cerebral insulin resistance, which causes neuronal degeneration, are so close that AD is sometimes referred to as 'type 3 diabetes'. Although the latest news on the therapeutic front for AD is encouraging, no treatment has been shown to halt disease progression permanently. At best, the treatments slow down the progression; at worst, they are inactive, or cause worrying side effects, preventing their use on a larger scale. Therefore, it appears logical that optimizing the metabolic milieu through preventive or curative measures can also slow down the cerebral degeneration that characterizes AD. Among the different classes of hypoglycaemic drugs, glucagon-like peptide 1 receptor agonists, which are widely used in the treatment of T2DM, were shown to slow down, or even prevent, neuronal degeneration. Data from animal, preclinical, clinical phase II, cohort and large cardiovascular outcomes studies are encouraging. Of course, randomized clinical phase III studies, which are on-going, will be essential to verify this hypothesis. Thus, for once, there is hope for slowing down the neurodegenerative processes associated with diabetes, and that hope is the focus of this review.

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