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.
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