dopa decarboxylase/atrofi

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Studies on the enzymatic blood-brain barrier: quantitative measurements of DOPA decarboxylase in the wall of microvessels as related to the parenchyma in various CNS regions.

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The presence of DOPA decarboxylase in cerebral microvessels (capillaries and venules) impedes the passage of circulating amine precursors into the brain. The relative amount of DOPA decarboxylase in this trapping mechanism as compared to the parenchyma per se was estimated in various CNS regions,

Parkinson's Disease: Recent Updates in the Identification of Human Dopa Decarboxylase Inhibitors.

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Backround: Parkinson's disease is a pathology involving the progressive degeneration of dopaminergic neurons in the substantia nigra of the brain. L-DOPA combined with an inhibitor of DOPA decarboxylase, a pyridoxal 5'-phosphate-dependent enzyme, is still the most effective treatment for symptoms of

Bax-inhibitor-1 knockdown phenotypes are suppressed by Buffy and exacerbate degeneration in a Drosophila model of Parkinson disease.

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BACKGROUND Bax inhibitor-1 (BI-1) is an evolutionarily conserved cytoprotective transmembrane protein that acts as a suppressor of Bax-induced apoptosis by regulation of endoplasmic reticulum stress-induced cell death. We knocked down BI-1 in the sensitive dopa decarboxylase (Ddc) expressing neurons

Treatment of idiopathic parkinsonism with L-dopa in the absence and presence of decarboxylase inhibitors: effects on plasma levels of L-dopa, dopa decarboxylase, catecholamines and 3-O-methyl-dopa.

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The effect of levodopa (L-dopa), alone or in combination with a peripheral decarboxylase inhibitor (PDI), on plasma levels of aromatic-L-amino acid decarboxylase (ALAAD, = dopa decarboxylase), L-dopa, 3-O-methyl-dopa (3-OMD), dopamine (DA), noradrenaline, adrenaline and dopamine beta-hydroxylase has

Longevity manipulations differentially affect serotonin/dopamine level and behavioral deterioration in aging Caenorhabditis elegans.

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Aging is accompanied with behavioral and cognitive decline. Changes in the neurotransmitter level are associated with the age-related behavioral deterioration, but whether well-known longevity manipulations affect the function of neurotransmitter system in aging animals is largely unclear. Here we

Biochemical and computational approaches to improve the clinical treatment of dopa decarboxylase-related diseases: an overview.

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Dopa decarboxylase (DDC) is a pyridoxal 5'-phosphate (PLP)-dependent enzyme that by catalyzing the decarboxylation of L-Dopa and L-5-hydroxytryptophan produces the neurotransmitters dopamine and serotonin. The functional properties of pig kidney and human DDC enzymes have been extensively

[Striato-nigral degeneration. Clinical and anatomic study of a case which responded favorably to L-Dopa].

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The authors have reported the case of a 65 year old woman followed for almost 4 years with an akineticrigid Parkinsonian syndrome which responded well to levodopa. Waning of response finally occurred and despite the addition of a peripheral dopa decarboxylase inhibitor the patient died suddenly.

Failure of vitamin B6 to reverse the L-dopa effect in patients on a dopa decarboxylase inhibitor.

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Seven patients with Parkinsonism previously on l-dopa were placed on a regimen of l-dopa and alpha methyl dopa hydrazine (a dopa decarboxylase inhibitor). Two of these patients had previously shown marked clinical deterioration of the l-dopa improvement when given pyridoxine. None of the seven

Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy.

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We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of

Differential and tissue-specific expression of a gene family for tyrosine/dopa decarboxylase in opium poppy.

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Two early and potential rate-limiting steps in the biosynthesis of isoquinoline alkaloids, such as morphine and codeine, in opium poppy (Papaver somniferum) involve decarboxylation of L-tyrosine and L-dihydroxyphenylalanine (L-dopa) to yield tyramine and dopamine, respectively. A DNA fragment was

Efficacy and tolerability of entacapone as adjunctive therapy to levodopa in patients with Parkinson's disease and end-of-dose deterioration in daily medical practice: an open, multicenter study.

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Entacapone is a potent, reversible and orally active inhibitor of catechol-O-methyltransferase. This open multicenter study evaluated the efficacy, safety and tolerability of entacapone as adjunct therapy to levodopa/dopa decarboxylase inhibitor (> or = 3 daily doses) in patients with idiopathic

Distribution of glutamic acid decarboxylase mRNA in the forebrain of the rainbow trout as studied by in situ hybridization.

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By using degenerate primers designed from glutamate decarboxylase (GAD) sequences of mammals, Xenopus and Drosophila, a 270-bp cDNA fragment was cloned by reverse transcriptase-polymerase chain reaction (RT-PCR) from cerebellum total RNA of rainbow trout. This partial cDNA shows 90% identity with

Sustained low-dose levodopa therapy in Parkinson's disease: a 3-year follow-up.

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Forty-four previously untreated patients with early idiopathic Parkinson's disease were treated from the time of diagnosis with submaximum doses of levodopa (mean 420 mg) in combination with a peripheral dopa decarboxylase inhibitor and followed for a minimum period of 3 years. Forty-one gained

Quinolinic acid: effects on brain catecholamine and c-AMP content during L-dopa and reserpine administration.

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The catecholamine content in rat brain tissue was determined following the administration of quinolinic acid alone or combined either with L-dopa and decarboxylase inhibitor or reserpine. Quinolinic acid alone decreased the levels of dopamine and noradrenaline, as well as those of c-AMP, and

[Recent progress in development of psychotropic drugs (3)--Antiparkinsonian agents applied in the treatment of Parkinson's disease or are under investigation for patients or model animals].

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Tremor, akinesia, rigidity and postual instability are key signs of Parkinson's disease. The most important one is akinesia, which includes decreased spontaneous locomotor activity, slowness of movement, awkwardness and freezing. On the other hand, an electrical focal lesion in the brain, neurotoxin

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