Shared dysregulated pathways lead to Parkinson's disease and diabetes

被引:211
作者
Santiago, Jose A. [1 ]
Potashkin, Judith A. [1 ]
机构
[1] Rosalind Franklin Univ Med & Sci, Chicago Med Sch, Cellular & Mol Pharmacol Dept, N Chicago, IL USA
关键词
Parkinson's disease; diabetes; insulin resistance; neurodegeneration; INDUCED INSULIN-RESISTANCE; GENOME-WIDE ASSOCIATION; GENE-EXPRESSION; ALPHA-SYNUCLEIN; PPAR-GAMMA; MITOCHONDRIAL DYSFUNCTION; NEUROTROPHIC FACTOR; GLUCOSE-METABOLISM; SUBSTANTIA-NIGRA; OXIDATIVE STRESS;
D O I
10.1016/j.molmed.2013.01.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Recent evidence indicates that Parkinson's disease and diabetes, both age-related chronic diseases, share remarkably similar dysregulated pathways. Exposure to environmental factors and genetic susceptibility play a role in the etiology and progression of both diseases. In light of recent findings, an intriguing hypothesis has emerged that suggests that mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and alterations in metabolism may lead to insulin resistance and, ultimately, to diabetes and/or neurodegeneration. In this article, we summarize the studies that have addressed the relationship between Parkinson's disease and diabetes and propose that disruptions in these shared molecular networks lead to both chronic diseases.
引用
收藏
页码:176 / 186
页数:11
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