caa a22 4500 606177485 CHVBK 20210128100752.0 cr unu---uuuuu 210128e20150601xx s 000 0 eng 10.1007/s00018-015-1854-x doi (NATIONALLICENCE)springer-10.1007/s00018-015-1854-x Molecular imaging of levodopa-induced dyskinesias [Elektronische Daten] [Flavia Niccolini, Lorenzo Rocchi, Marios Politis] Levodopa-induced dyskinesias (LIDs) occur in the majority of patients with Parkinson's disease (PD) following years of levodopa treatment. The pathophysiology underlying LIDs in PD is poorly understood, and current treatments generate only minor benefits for the patients. Studies with positron emission tomography (PET) molecular imaging have demonstrated that in advanced PD patients, levodopa administration induces sharp increases in striatal dopamine levels, which correlate with LIDs severity. Fluctuations in striatal dopamine levels could be the result of the attenuated buffering ability in the dopaminergically denervated striatum. Lines of evidence from PET studies indicate that serotonergic terminals could also be responsible for the development of LIDs in PD by aberrantly processing exogenous levodopa and by releasing dopamine in a dysregulated manner from the serotonergic terminals. Additionally, other downstream mechanisms involving glutamatergic, cannabinoid, opioid, cholinergic, adenosinergic, and noradrenergic systems may contribute in the development of LIDs. In this article, we review the findings from preclinical, clinical, and molecular imaging studies, which have contributed to our understanding the pathophysiology of LIDs in PD. Springer Basel, 2015 Dyskinesias nationallicence Graft-induced dyskinesias nationallicence Levodopa-induced dyskinesias nationallicence Parkinson's disease nationallicence PET nationallicence GIDs : Graft-induced dyskinesias nationallicence LIDs : Levodopa-induced dyskinesias nationallicence PET : Positron emission tomography nationallicence PD : Parkinson's disease nationallicence Niccolini Flavia Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, SE5 8AF, London, UK aut Rocchi Lorenzo Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, SE5 8AF, London, UK aut Politis Marios Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, SE5 8AF, London, UK aut Cellular and Molecular Life Sciences Springer Basel 72/11(2015-06-01), 2107-2117 1420-682X 72:11<2107 2015 72 18 https://doi.org/10.1007/s00018-015-1854-x text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 review-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00018-015-1854-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Niccolini Flavia Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, SE5 8AF, London, UK aut NATIONALLICENCE 700 1- Rocchi Lorenzo Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, SE5 8AF, London, UK aut NATIONALLICENCE 700 1- Politis Marios Neurodegeneration Imaging Group, Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London, SE5 8AF, London, UK aut NATIONALLICENCE 773 0- Cellular and Molecular Life Sciences Springer Basel 72/11(2015-06-01), 2107-2117 1420-682X 72:11<2107 2015 72 18