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Paper Details

GCH1 Deficiency Activates Brain Innate Immune Response and Impairs Tyrosine Hydroxylase Homeostasis.
J Neurosci
7
2022
BH4, DRD, GCH1, GCH1 deficiency, GTP, GTP cyclohydrolase 1, GTP cyclohydrolase I, GWAS risk factors, GWAS risk genes, L-Dopa, PD, Parkinson's disease, Tyrosine, Tyrosine hydroxylase protein, Zebrafish, ascending dopaminergic (DAergic) neurons, dopa, dopa-responsive dystonia, dopamine, dopaminergic, dopaminergic cell death, gch1, gch1 larvae, genetic risk factors, larval, lethality, microglial, monoaminergic neurotransmitter deficiencies, movement deficits, neuronal cell, non-neurodegenerative movement disorder, parkinsonism, sporadic Parkinson's disease, tetrahydrobiopterin, tyrosine, tyrosine hydroxylase, zebrafish, zebrafish gch1 mutant
Author NameAffiliation
Wenbin WeiSheffield Institute for Translational Neuroscience (SITraN), University of Sheffield
Winston HideSheffield Institute for Translational Neuroscience (SITraN), University of Sheffield
Winston HideBeth Israel Medical Center
Winston HideHarvard Medical School
Winston HideSheffield Institute for Translational Neuroscience (SITraN), University of Sheffield
Winston HideBeth Israel Medical Center
Winston HideHarvard Medical School
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