Abstract
Cancer and neurodegeneration are two major leading causes of morbidity and death worldwide. At first sight, the two fields do not seem to share much in common and, if anything, might be placed on opposite ends of a spectrum. Although neurodegeneration results in excessive neuronal cell death, cancer emerges from increased proliferation and resistance to cell death. Therefore, one might expect significant differences in the underlying pathophysiological mechanisms. However, the more we deepen our understanding of these two types of diseases, the more we appreciate the unexpected overlap between them. Although most epidemiological studies support an inverse association between the risk for development of neurodegenerative diseases and cancer, increasing evidence points to a positive correlation between specific types of cancer, like melanoma, and neurodegenerative diseases, like Parkinson's disease (PD). We believe that deciphering the molecular processes and pathways underlying one of these diseases may significantly increase our understanding about the other. Therefore, the identification of novel biomarkers and therapeutic approaches in cancer, may lead to improved diagnosis and treatment of neurodegeneration, and vice versa. In this Viewpoint, we summarize recent findings connecting both diseases and speculate that insights from one disease may inform on mechanisms, and help identify novel biomarkers and targets for intervention, possibly leading to improved management of both diseases.
Original language | English |
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Pages (from-to) | 340-346 |
Number of pages | 7 |
Journal | Movement Disorders |
Volume | 36 |
Issue number | 2 |
DOIs | |
Publication status | Published - 21 Dec 2020 |
Bibliographical note
Funding Information:T.F.O. is supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy (EXC 2067/1‐ 390729940).
Publisher Copyright:
© 2020 International Parkinson and Movement Disorder Society
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.