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Autonomic dysfunction in Parkinson disease and animal models

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Abstract

Parkinson disease has traditionally been classified as a movement disorder, despite patients’ accounts of diverse symptoms stemming from impairments in numerous body systems. Today, Parkinson disease is increasingly recognized by clinicians and scientists as a complex neurodegenerative disorder featuring both motor and nonmotor manifestations concomitant with pathology throughout all major branches of the nervous system. Dysfunction of the autonomic nervous system, or dysautonomia, is a common feature of Parkinson disease. It produces signs and symptoms that severely affect patients’ quality of life, such as blood pressure dysregulation, hyperhidrosis, and constipation. Treatment options for dysautonomia are limited to symptom alleviation because the cause of these symptoms and Parkinson disease overall are still unknown. Animal models provide a platform to interrogate mechanisms of Parkinson disease-related autonomic nervous system dysfunction and test novel treatment strategies. Several animal models of Parkinson disease are available, each with different effects on the autonomic nervous system. This review critically analyses key dysautonomia signs and symptoms and associated pathology in Parkinson disease patients and relevant findings in animal models. We focus on the cardiovascular system, adrenal medulla, skin/thermoregulation, bladder, pupils, and gastrointestinal tract, to assess the contribution of animal models to the understanding of Parkinson disease autonomic dysfunction.

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Acknowledgements

This research was supported by grants National Institutes of Health (NIH) P51OD011106, NIH R24OD019803, NIH Kirschstein-NRSA F31HL136047 (J.M.M), and the University of Wisconsin–Madison Office of Vice Chancellor for Research and Graduate Education, Cellular and Molecular Pathology Graduate Program, and Department of Medical Physics.

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Metzger, J.M., Emborg, M.E. Autonomic dysfunction in Parkinson disease and animal models. Clin Auton Res 29, 397–414 (2019). https://doi.org/10.1007/s10286-018-00584-7

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