Type 2 Diabetes Mellitus Exacerbates Pathological Processes of Parkinson's Disease: Insights from Signaling Pathways Mediated by Insulin Receptors
Shufen Liu1,2 · Tingting Liu1,2 · Jingwen Li2 · Jun Hong2 · Ali A. Moosavi‑Movahedi3 · Jianshe Wei1,2 1 Center for Translational Neuromedicine and Neurology, School of Life Sciences, Institute for Brain Sciences Research, Henan University, Huaihe Hospital of Henan University, Kaifeng 475004, China
2 School of Life Sciences, Institute for Brain Sciences Research, Henan University, Kaifeng 475004, China
3 Institute of Biochemistry and Biophysics, University of Tehran, Tehran 999067, Iran
Abstract
Parkinson’s disease (PD), a chronic and common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the dense part of the substantia nigra and abnormal aggregation of alpha-synuclein. Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by chronic insulin resistance and deficiency in insulin secretion. Extensive evidence has confirmed shared pathogenic mechanisms underlying PD and T2DM, such as oxidative stress caused by insulin resistance, mitochondrial dysfunction, inflammation, and disorders of energy metabolism. Conventional drugs for treating T2DM, such as metformin and glucagon-like peptide-1 receptor agonists, affect nerve repair. Even drugs for treating PD, such as levodopa, can affect insulin secretion. This review summarizes the relationship between PD and T2DM and related therapeutic drugs from the perspective of insulin signaling pathways in the brain.
Keywords
Parkinson’s disease; Type 2 diabetes mellitus; Insulin; Therapeutic agents
