Shared dysregulated pathways lead to Parkinson's disease and diabetes

Trends Mol Med. 2013 Mar;19(3):176-86. doi: 10.1016/j.molmed.2013.01.002. Epub 2013 Jan 31.


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.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Biomarkers / blood
  • Blood Glucose / analysis
  • Chronic Disease
  • Diabetes Mellitus / genetics*
  • Diabetes Mellitus / physiopathology
  • Disease Progression
  • Endoplasmic Reticulum Stress
  • Genetic Predisposition to Disease
  • Homeostasis
  • Humans
  • Inflammation / genetics
  • Inflammation / physiopathology
  • Insulin Resistance / genetics
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism
  • Mitochondria / metabolism
  • Parkinson Disease / genetics*
  • Parkinson Disease / physiopathology
  • Transcription Factors
  • Vitamin D / pharmacology


  • Biomarkers
  • Blood Glucose
  • Transcription Factors
  • Vitamin D
  • Insulin-Like Growth Factor I