Pentose-phosphate pathway disruption in the pathogenesis of Parkinson’s disease

Laura Dunn 1 , Vanessa Fairfield 1 , Shanay Daham 1 , Juan Bolaños 2 ,  and Simon Heales
  • 1 Undergraduate School of Medicine, Imperial College London, South Kensington Campus, London, SW7 2AZ, UK
  • 2 Institute of Functional Biology and Genomics, University of Salamanca — Consejo Superior de Investigaciones Científicas, 37007, Salamanca, Spain
  • 3 Chemical Pathology Department, Great Ormond Street Hospital, London, WC1N 1LE, UK
  • 4 Centre for Translational Genomics, University College London, Institute of Child Health, London, WC1N 1EH, UK
  • 5 Department of Molecular Neuroscience, University College London, Institute of Neurology, Queen Square, London, WC1N 6BG, UK

Abstract

Oxidative stress is known to be a key factor in the pathogenesis of Parkinson’s disease (PD). Neuronal redox status is maintained by glucose metabolism via the pentose-phosphate pathway and it is known that disruption of glucose metabolism is damaging to neurons. Accumulating evidence supports the idea that glucose metabolism is altered in PD and dysregulation of the pentose-phosphate pathway in this disease has recently been shown. In this review, we present an overview of the literature regarding neuronal glucose metabolism and PD, and discuss the implications of these findings for PD pathogenesis and possible future therapeutic avenues.

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