Insulin Resistance and Alzheimer's Disease: Bioenergetic Linkages.
Insulin Resistance and Alzheimer's Disease: Bioenergetic Linkages.
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DOI：
10.3389/fnagi.2017.00345
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发表时间：
2017
影响因子：
4.8
通讯作者：
Craft S
中科院分区：
文献类型：
--
作者：
Neth BJ;Craft S
代谢功能障碍是阿尔茨海默病（AD）的一个明确特征，可以在AD症状发生前数十年观察到脑葡萄糖代谢低下。此外，越来越多的人支持代谢性疾病与AD和相关痴呆症的发展之间的关联。患有胰岛素抵抗、2型糖尿病（T2D）、高脂血症、肥胖或其他代谢疾病的个体可能会增加AD和类似疾病（如血管性痴呆）的风险。这种关联可能部分是由于这些病理常见的全身性线粒体功能障碍。越来越多的证据表明，线粒体功能障碍是AD的一个重要特征，并可能在其发病机制中发挥重要作用。事实上，由于固有的线粒体功能障碍和慢性代谢疾病的流行，衰老本身提出了一个独特的挑战。尽管在了解AD的发病机制和开发潜在疗法方面取得了进展，但目前我们仍然没有改善疾病的治疗方法。在这篇综述中，我们将讨论胰岛素抵抗作为AD发病机制的一个因素，以及胰岛素抵抗和AD之间的代谢和生物能量破坏。我们还将专注于潜在的神经影像学工具，用于研究AD中常见的代谢功能障碍，并希望开发治疗和预防目标。
Metabolic dysfunction is a well-established feature of Alzheimer’s disease (AD), evidenced by brain glucose hypometabolism that can be observed potentially decades prior to the development of AD symptoms. Furthermore, there is mounting support for an association between metabolic disease and the development of AD and related dementias. Individuals with insulin resistance, type 2 diabetes mellitus (T2D), hyperlipidemia, obesity, or other metabolic disease may have increased risk for the development of AD and similar conditions, such as vascular dementia. This association may in part be due to the systemic mitochondrial dysfunction that is common to these pathologies. Accumulating evidence suggests that mitochondrial dysfunction is a significant feature of AD and may play a fundamental role in its pathogenesis. In fact, aging itself presents a unique challenge due to inherent mitochondrial dysfunction and prevalence of chronic metabolic disease. Despite the progress made in understanding the pathogenesis of AD and in the development of potential therapies, at present we remain without a disease-modifying treatment. In this review, we will discuss insulin resistance as a contributing factor to the pathogenesis of AD, as well as the metabolic and bioenergetic disruptions linking insulin resistance and AD. We will also focus on potential neuroimaging tools for the study of the metabolic dysfunction commonly seen in AD with hopes of developing therapeutic and preventative targets.
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影响因子：
3.8
作者：
Adibhatla RM;Hatcher JF
通讯作者：
Hatcher JF
影响因子：
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作者：
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通讯作者：
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Erickson, Michelle A.