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| http://dx.doi.org/10.1136/bcr-2016-215859 | DOI Listing |
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Differential Activation States of Direct Pathway Striatal Output Neurons during l-DOPA-Induced Dyskinesia Development.
J Neurosci
June 2024
Department of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, Alabama 35294
l-DOPA-induced dyskinesia (LID) is a debilitating motor side effect arising from chronic dopamine (DA) replacement therapy with l-DOPA for the treatment of Parkinson's disease. LID is associated with supersensitivity of striatal dopaminergic signaling and fluctuations in synaptic DA following each l-DOPA dose, shrinking the therapeutic window. The heterogeneous composition of the striatum, including subpopulations of medium spiny output neurons (MSNs), interneurons, and supporting cells, complicates the identification of cell(s) underlying LID.
View Article and Find Full Text PDFDystonic crises in dopa-responsive dystonia induced by energy drinks.
Pract Neurol
June 2019
Alfred Hospital, Melbourne, Victoria, Australia.
We present an interesting case of recurrent dystonic crises in dopa-responsive dystonia (DRD) likely induced by excessive consumption of aspartame-containing products, in particular sugar-free energy drinks. This has a strong practical value as acute presentations to the emergency department can be avoided in these susceptible individuals. Usual medical and dietary advice in the treatment of DRD would include the avoidance of high-dose phenylalanine-containing products, and to this we would advocate the avoidance of high-dose aspartame-containing products.
View Article and Find Full Text PDFGCH1 variants, tetrahydrobiopterin and their effects on pain sensitivity.
Scand J Pain
April 2014
Applied Human Molecular Genetics, Kennedy Center, Copenhagen University Hospital, Rigshospitalet, Glostrup, Denmark.
Background A great proportion of the variation in pain experience and chronicity is caused by heritable factors. Within the last decades several candidate genes have been discovered either increasing or decreasing pain sensitivity or the risk of chronic pain in humans. One of the most studied genes is the GCH1 gene coding for the enzyme GTP cyclohydrolase 1 (GCH1).
View Article and Find Full Text PDFHeterozygous mutations in GTP-cyclohydrolase-1 reduce BH4 biosynthesis but not pain sensitivity.
Pain
June 2018
Applied Human Molecular Genetics, Clinical Genetic Clinic, Kennedy Center, Copenhagen University Hospital, Rigshospitalet, Glostrup, Denmark.
Human studies have demonstrated a correlation between noncoding polymorphisms of "the pain protective" haplotype in the GCH1 gene that encodes for GTP cyclohydrolase I (GTPCH1)-which leads to reduced tetrahydrobiopterin (BH4) production in cell systems-and a diminished perception of experimental and clinical pain. Here, we investigate whether heterozygous mutations in the GCH1 gene which lead to a profound BH4 reduction in patients with dopa-responsive dystonia (DRD) have any effect on pain sensitivity. The study includes an investigation of GCH1-associated biomarkers and pain sensitivity in a cohort of 22 patients with DRD and 36 controls.
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BMJ Case Rep
June 2016
Department of Neurology, Tokyo Metropolitan Neurological Hospital, Fuchu, Tokyo, Japan.
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