Striatal Overexpression of ΔJunD Resets L-DOPA-Induced Dyskinesia in a Primate Model of Parkinson Disease

Involuntary movements, or dyskinesia, represent a debilitating complication of dopamine replacement therapy for Parkinson disease (PD). The transcription factor ΔFosB accumulates in the denervated striatum and dimerizes primarily with JunD upon repeated L-3,4-dihydroxyphenylalanine (L-DOPA) administ...

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Veröffentlicht in:	Biological psychiatry (1969) Jg. 66; H. 6; S. 554 - 561
Hauptverfasser:	Berton, Olivier, Guigoni, Céline, Li, Qin, Bioulac, Bernard H., Aubert, Incarnation, Gross, Christian E., DiLeone, Ralph J., Nestler, Eric J., Bezard, Erwan
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	New York, NY Elsevier Inc 2009 Elsevier
Schlagworte:	AAV Adult and adolescent clinical studies Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases dyskinesia L-DOPA LID Medical sciences Nervous system (semeiology, syndromes) Nervous system as a whole Neurology Organic mental disorders. Neuropsychology Parkinson disease Psychiatric/Mental Health Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry ΔFosB ΔJunD ΔFosB AAV LID L-DOPA Parkinson disease ΔJunD dyskinesia Agonist Central nervous system Gene overexpression Cognition Encephalon Involuntary movement Primates Degenerative disease Levodopa Neurological disorder Motricity Dyskinesia Nervous system diseases Basal ganglion Corpus striatum Antiparkinson agent Motor control Cerebral disorder Vertebrata Mammalia D2 Dopamine receptor Central nervous system disease Models Extrapyramidal syndrome
ISSN:	0006-3223, 1873-2402
Online-Zugang:	Volltext
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