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- W2290597782 abstract "Parkinson's disease (PD) is a neurological disorder resulting from a deficiency of dopamine (DA) in the neostriatum due to degeneration of dopaminergic neurons in the substantia nigra. The major therapeutic drug for PD is L-3,4-dihydroxyphenylalanine (L-DOPA), which is the precursor of DA. However, long-term treatment of L-DOPA induces side effects including dyskinesias, wearing-off and on-off phenomenon. Previous studies in our lab led to investigation of the metabolic events of L-DOPA treatment, including the role of L-dopa on L-aromatic amino acid decarboxylase (LAAD), the enzyme that catalyzes the formation of DA from L-DOPA. In this project we prepare 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) PD disease mouse model and treat them with L-dopa at 100 mg/kg. We studied the locomotor activity of the mice and performed Western blot assay for LAAD. The results showed that the sub-chronic administration of L-DOPA decreased LAAD expression in the striatum of the MPTP-PD mouse model, but increased it in the cortex. L-DOPA generates high amounts of DA, therefore, the data suggest that DA causes a feedback or allosteric downregulation of striatal LAAD. This down-regulation of LAAD may contribute to the wearing-off phenomenon and may show that the key side effects of L-dopa may be due to the disturbance of the homeostasis of the catecholamine enzymes by the overload of L-DOPA." @default.
- W2290597782 created "2016-06-24" @default.
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- W2290597782 date "2008-03-01" @default.
- W2290597782 modified "2023-09-27" @default.
- W2290597782 title "Modulation of of l‐Aromatic Amino Acid Decarboxylase by 3, 4‐dihydroxyphenylalanine in the MPTP mouse model." @default.
- W2290597782 doi "https://doi.org/10.1096/fasebj.22.1_supplement.715.3" @default.
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