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Biomedical subjects

Y Agid

Publications and source records attributed to Y Agid.

At least 559 records · Page 31Linked to original sources
PubMed1981

Bromocriptine in Parkinson's disease: a study of cardiovascular effects.

Blood pressure and pulse rate were studied in 20 Parkinsonian patients on no treatment, and during treatment with bromocriptine (mean dosage 148 mg/day) as the sole anti-Parkinsonian therapy. The drug was shown to reduce erect systolic and diastolic and supine systolic blood pressure and to increase erect pulse rate, in a predictable dose-dependent manner. The occurrence of episodes of significant postural hypotension was less predictable and was a transitory phenomenon in all patients. Peripheral dopamine receptor blockade with domperidone did not alter the findings, suggesting that the principal mechanism for these cardiovascular effects is a central dopaminergic one.

Benzimidazoles↗
PubMed1981

Treatment of Huntington disease with gamma-acetylenic GABA an irreversible inhibitor of GABA-transaminase: increased CSF GABA and homocarnosine without clinical amelioration.

gamma-Acetylenic GABA (GAG, RMI 71.645), a potent irreversible inhibitor of gamma-aminobutyric acid transaminase, was given orally in various dosage schedules to 14 patients with Huntington disease. The biochemical effects of the drug on cerebrospinal fluid (CSF) concentrations of gamma-aminobutyric acid (GABA) and the GABA-containing dipeptide, homocarnosine, were measured in 10 of 14 patients. Treatment with GAG increased CSF concentrations of GABA and homocarnosine as compared to pretreatment values, suggesting that the drug increased brain GABA concentration. Despite this neurochemical effect, the clinical state was not improved. Except for single seizure episodes in five patients, GAG therapy was well tolerated. These results do not exclude the possibility that agents that augment CNS GABAergic function may prove useful in therapy of Huntington disease.

4-Aminobutyrate Transaminase↗
PubMed1981

Bromocriptine and domperidone in the treatment of Parkinson disease.

In a single-blind trial of therapy in 20 patients with idiopathic Parkinson disease, domperidone prevented nausea and vomiting induced by bromocriptine without diminishing beneficial central effects. Combination of the two drugs permitted rapid increase in bromocriptine dosage from 22.5 mg per day to 148 mg per day, with 71% mean clinical improvement over baseline score; continuing efficacy of the regimen was evident for a mean follow-up of 2 months.

Benzimidazoles↗
PubMed1980

L-Histidine decarboxylase in the human brain: properties and localization.

The properties of the histamine-forming enzyme in human brain samples were studied utilizing a radiochromatographic procedure. The influence of postmortem conditions was checked with rat brains, and the results indicated that the enzyme activity is not altered in situ for a delay not exceeding 4 h at ambient temperature. Moreover, tissue blocks or homogenates can be stored at temperatures for up to 3 months with a good preservation of the enzyme activity. The data indicate that histamine synthesis in the human brain involves the "specific" histidine decarboxylase (HD, EC 4.1.1.22) and not the aromatic L-amino acid decarboxylase: (1) the optimum pH is 7.4 at 10(-6) M-L-histidine; (2) the apparent Km is about 3.10(-5) M; (3) it is inhibited by alpha-hydrazino histidine and brocresine but not affected by alpha-methyl DOPA. Moreover, a major portion of the enzyme is localized in a subcellular fraction containing nerve terminals and it shows an uneven regional distribution which parallels that observed in the brain of other mammalian species. Taken together these data strongly suggest that histamine could play a neurotransmitter role in the human brain.

Aged↗
PubMed1980

Is the mesocortical dopaminergic system involved in Parkinson disease?

Tyrosine hydroxylase was used to identify catecholaminergic neurons in the substantia nigra and ventral tegmental area of the human mesencephalon. High enzyme activity in the normal ventral tegmental area indicated the presence of numerous cathecholaminergic neurons, most likely dopamine cells. Tyrosine-hydroxylase activity was decreased in the ventral tegmental area of parkinsonian patients, implying a lesion of the mesocortical dopamine system in Parkinson disease.

Aged↗
PubMed1979

[Acetylcholine receptors (author's transl)].

The actions of acetylcholine can be classified as nicotine-like or muscarine-like. Nicotinic actions of acetylcholine are seen at the skeletal neuromuscular junction and at autonomic ganglia whereas muscarinic transmission occurs at parasympathetic effector organs and in the brain. The sites on the membrane surface of a neuronal cell body or dendrite where acetylcholine acts is called a receptor site. There has been marked progress in the last few years in the identification and quantification of acetylcholine receptors by biochemical methods by means of specific radioactive ligands of very high activity and very high affinity for these receptors. Using these techniques it has been possible to: determine the regional distribution of nicotinic and muscarinic receptors in the brain, evaluate new drugs acting on these receptors, and determine the concentration of these receptors in neurologic disorders.

Acetylcholine↗
PubMed1979

Nerve growth factor (NGF) in the rat CNS: absence of specific retrograde axonal transport and tyrosine hydroxylase induction in locus coeruleus and substantia nigra.

Selective, highly efficient uptake of [125I]NGF by nerve terminals followed by retrograde axonal transport, and specific induction of tyrosine hydroxylase by NGF are well known phenomena in peripheral adrenergic neurons of adult rats. In the present study these parameters were used in order to detect possible interactions of NGF with central catecholaminergic neurons. No selective retrograde transport of [125I]NGF could be detected by light microscopic autoradiography from the caudate nucleus to the dopaminergic neurons in the substantia nigra or from the hippocampus to the noradrenergic nerve cells of the locus coeruleus. Biochemically, no change in tyrosine hydroxylase activity could be observed for up to 3 days after injection of either NGF, anti-NGF antibodies, or control proteins close to the nerve cell bodies in the substantia nigra or the locus coeruleus. These data suggest a fundamental difference between central and peripheral adrenergic neurons with regard to their responsiveness of NGF.

Adrenergic Fibers↗
PubMed1979

Bromocriptine associated with a peripheral dopamine blocking agent in treatment of Parkinson's disease.

A peripheral dopaminergic blocking agent, domperidone (60 mg daily), or placebo was given, double-blind, to 17 parkinsonian patients who also received increasing doses of bromocriptine. Combined treatment with domperidone reduced total disability by 76% in 8 patients receiving a mean dose of 148 mg of bromocriptine daily. There was no vomiting and involuntary movements and psychic disturbances were similar to those in patients on levodopa and a peripheral decarboxylase inhibitor. In 9 patients taking placebo instead of domperidone, the average daily dose of bromocriptine could not be raised beyond 92 mg. The mean total disability score in this group was reduced by only 48%. Thus, peripheral blockade of dopamine receptors is a promising means of limiting the adverse side-effects of the treatment of parkinsonism with central dopaminergic receptor stimulating agents such as bromocriptine.

Adult↗
PubMed1979

[Influence of choline on amnesia in Alzheimer's disease (author's transl)].

Eight patients with Alzheimer's disease presenting whith memory difficulties and no significant intellectual deterioration were treated with 9 grams daily. Choline base orally for 3 weeks. Quantitative testing, which evaluate memory capabilities such as learning and recall after delays of 1 hour and 24 hours, were used before and after the administration of Choline. The results of a global statistical analysis did not show any significant difference in the performances obtained before and after choline. However, in two patients, recall performance improvement was confirmed clinically. Most likely, these two patients were suffering from an mild foorm of Alzheimer's disease.

Aged↗