System-based approaches to decode the molecular links in Parkinson's disease and diabetes.
A growing body of evidence indicates an increased risk for developing Parkinson's disease (PD) among people with type 2 diabetes (T2DM). The relationship between the etiology and development of both chronic diseases is beginning to be uncovered and recent studies show that PD and T2DM share remarkably similar dysregulated pathways. It has been proposed that a cascade of events including mitochondrial dysfunction, impaired insulin signaling, and metabolic inflammation trigger neurodegeneration in T2DM models. Network-based approaches have elucidated a potential molecular framework linking both diseases. Further, transcriptional signatures that modulate the neurodegenerative phenotype in T2DM have been identified. Here we contextualize the current experimental approaches to dissect the mechanisms underlying the association between PD and T2DM and discuss the existing challenges toward the understanding of the coexistence of these devastating aging diseases.
The Cellular and Molecular Pharmacology Department, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Jose A
JA
Santiago
The Cellular and Molecular Pharmacology Department, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA. Electronic address: judy.potashkin@rosalindfranklin.edu.
Judith A
JA
Potashkin
D000818:Animals; D015415:Biomarkers / Q000097:blood; D016208:Databases, Factual; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000235:genetics* / Q000378:metabolism*; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008957:Models, Genetic; D010300:Parkinson Disease / Q000150:complications* / Q000235:genetics* / Q000378:metabolism*; D012307:Risk Factors
D015415:Biomarkers
Inflammation; Insulin resistance; Neurodegeneration; Parkinson's disease; Type 2 diabetes