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Association Between Pathophysiological Mechanisms of Diabetic Retinopathy and Parkinson’s Disease

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Abstract

Diabetic retinopathy, the most common complication of diabetes, is a neurodegenerative disease in the eye. And Parkinson's disease, affecting the health of 1–2% of people over 60 years old throughout the world, is the second largest neurodegenerative disease in the brain. As the understanding of diabetic retinopathy and Parkinson's disease deepens, the two diseases are found to show correlation in incidence, similarity in clinical presentation, and close association in pathophysiological mechanisms. To reveal the association between pathophysiological mechanisms of the two disease, in this review, the shared pathophysiological factors of diabetic retinopathy and Parkinson's disease are summarized and classified into dopaminergic system, circadian rhythm, neurotrophic factors, α-synuclein, and Wnt signaling pathways. Furthermore, similar and different mechanisms so far as the shared pathophysiological factors of the two disorders are discussed systematically. Finally, a brief summary and new perspectives are presented to provide new directions for further efforts on the association, exploration, and clinical prevention and treatment of diabetic retinopathy and Parkinson's disease.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (Nos. 81660166 and 81660146), the Yunnan Science and Technology Talents and Platform Plan (No. 2019HB050), and Yunnan Youth Talent Support Program (No. YNWR-QNBJ-2018-315).

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ZQZ, YKZ and HYZ contributed equally to the paper. All authors read and approved of the final manuscript.

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Correspondence to Xiaochun Yang.

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The authors declare that there are no potential conflicts of interest.

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This work does not contain any studies with human participants or animals performed by any of the authors.

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Zhang, Z., Zhou, Y., Zhao, H. et al. Association Between Pathophysiological Mechanisms of Diabetic Retinopathy and Parkinson’s Disease. Cell Mol Neurobiol 42, 665–675 (2022). https://doi.org/10.1007/s10571-020-00953-9

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  • DOI: https://doi.org/10.1007/s10571-020-00953-9

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