DPP4 抑制剂可作为 3 型糖尿病的首选药物：小型综述。
DPP4 Inhibitors Can Be a Drug of Choice for Type 3 Diabetes: A Mini Review.
机构信息
1 Department of Pharmacognosy and Phytopharmacy, JSS College of Pharmacy, (Constituent College of Jagadguru Sri Shivarathreeswara University, Mysuru), Ooty, India.
2 Department of Pharmacology, Guntur Medical College, Guntur, Andhra Pradesh, India.
出版信息
Am J Alzheimers Dis Other Demen. 2017 Nov;32(7):444-451. doi: 10.1177/1533317517722005. Epub 2017 Jul 27.
Abstract
As well known to the scientific community, Alzheimer's disease (AD) is an irreversible neurodegenerative disease that ends up with impairment of memory and cognition due to neuronal and synapse loss. Patient's quality of life can be enhanced by targeting neurogenesis as a therapeutic paradigm. Moreover, several research evidences support the concept that AD is a type of metabolic disorder mediated by impairment in brain insulin responsiveness and energy metabolism. Growing evidence suggests that endogenous peptides such as glucagon-like peptide-1 (GLP-1) and stromal-derived factor-1α (SDF-1α) provide neuroprotection across a range of experimental models of AD. So, preserving functional activity of SDF-1α and GLP-1 by dipeptidyl peptidase-4 inhibition will enhance the homing/recruitment of brain resident and nonresident circulating stem cells/progenitor cells, a noninvasive approach for promoting neurogenesis. So, herewith we provide this in support of dipeptidyl peptidase-4 inhibitors as a new target of attention for treating AD.
摘要
科学界众所周知，阿尔茨海默病（AD）是一种不可逆转的神经退行性疾病，由于神经元和突触的丧失，最终导致记忆和认知障碍。通过将神经发生作为一种治疗范例，患者的生活质量可以得到提高。此外，多项研究证据支持这样一种概念，即 AD 是一种由脑胰岛素反应性和能量代谢受损介导的代谢障碍。越来越多的证据表明，内源性肽如胰高血糖素样肽-1（GLP-1）和基质衍生因子-1α（SDF-1α）在一系列 AD 实验模型中提供神经保护作用。因此，通过二肽基肽酶-4 抑制来保留 SDF-1α和 GLP-1 的功能活性，将增强脑内固有和非固有循环干细胞/祖细胞的归巢/募集，这是一种促进神经发生的非侵入性方法。因此，我们在此提供这方面的支持，认为二肽基肽酶-4 抑制剂是治疗 AD 的一个新的关注目标。
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