摘要
就目前的分析,我们旨在探索许多重要的机制,这些机制有助于弥补概念差距填充认识碎片,青光眼确实是大脑特定的糖尿病更准确地说是“四型糖尿病”。基于这种概念的实质,我们得出一个新的思路,关于胰岛素成为一种潜在的青光眼治疗法。这个分析综合了关于青光眼的大脑挑战、分离大脑糖尿病的可能性、青光眼方法学的胰岛素信号差错、线粒体的功能障碍和胰岛素抵抗青光眼、眼内压的胰岛素介导条件和它在线粒体功能障碍的失调方面出版的文献。我们也调查了青光眼的发病机制和胰岛素信号通路的作用。每走一步,讨论揭露了胰岛素和其他联合的部分有确定的前景治疗和管理青光眼。这篇文章,我们旨在综合一个有说服力的和包括一切的构图关于焦点在中枢神经系统“胰岛素低功能”的病因病机(例如大脑的特定糖尿病)。我们一开始考虑到神经组织性衰退糖尿病的可能,它独立存在于末梢神经性糖尿病。一旦满足条件,这种大脑特定糖尿病的代谢团块研讨导致我们理解视网膜神经节细胞凋亡的发展、眼内高压、视杯和线粒体功能障碍。所有的这些都是满足诊断青光眼标准的标志和必要条件。即刻应用这种分析观点治疗青光眼提高了被我们称之为胰岛素低功能的疾病。
关键词: 阿尔兹海默病,大脑,中枢神经系统,糖尿病,青光眼,炎症,胰岛素,胰岛素抵抗,眼内压,线粒体,神经组织衰退性疾病,神经节,视神经,视网膜。
Current Molecular Medicine
Title:Diabetes Type 4: A Paradigm Shift in the Understanding of Glaucoma, the Brain Specific Diabetes and the Candidature of Insulin as a Therapeutic Agent
Volume: 17 Issue: 1
关键词: 阿尔兹海默病,大脑,中枢神经系统,糖尿病,青光眼,炎症,胰岛素,胰岛素抵抗,眼内压,线粒体,神经组织衰退性疾病,神经节,视神经,视网膜。
摘要: In the present analysis, we aim at probing into many important mechanisms that serve to bridge conceptual gaps to fill up the mosaic of a picture revealing that glaucoma indeed is brain specific diabetes and more appropriately “Diabetes Type 4”. Based on this conceptual substance, we weave a novel idea of insulin being a potential remedy for glaucoma. This analysis synthesizes upon the published literature on brain changes in glaucoma, possibility of isolated brain diabetes, insulin signaling glitches in glaucoma pathology, mitochondrial dysfunction and insulin resistance in glaucomatous eyes, insulin mediated regulation of intraocular pressure and its dysregulation in mitochondrial dysfunction. We also look into the role of amyloidopathy and taupathy in glaucoma pathogenesis vis-à-vis insulin signaling. At every step, the discussion reveals that insulin and other allied moieties are a sure promise for glaucoma treatment and management. In this article, we aim at synthesizing a persuasive and all inclusive picture of glaucoma etiopathomechanism centered on “insulin-hypofunctionality” in the central nervous system (i.e. brain specific diabetes). We start with considering the possibility of neurodegenerative diabetes that exists independent of the peripheral diabetes. Once that condition is met, then a metabolic conglomeration of this brain specific diabetes is deliberated upon leading us to understand the development of retinal ganglion cell apoptosis, intraocular pressure elevation, optic cupping and mitochondrial dysfunction. All these are the hallmarks and sufficient conditions to satisfy the diagnostic criteria for glaucoma. Immediate application of this analysis points towards glaucoma therapy centered upon improving what we have termed insulin-hypofunctionality.
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Cite this article as:
Diabetes Type 4: A Paradigm Shift in the Understanding of Glaucoma, the Brain Specific Diabetes and the Candidature of Insulin as a Therapeutic Agent, Current Molecular Medicine 2017; 17 (1) . https://dx.doi.org/10.2174/1566524017666170206153415
DOI https://dx.doi.org/10.2174/1566524017666170206153415 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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