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Biomedical subjects

P Riederer

Publications and source records attributed to P Riederer.

At least 469 records · Page 26Linked to original sources
PubMed1983

General properties of 14C-L-Valine-binding to human brain tissue.

L-Valine (VAL) binding is saturable, reversible, linear within a protein concentration of 0.2 to 0.8 mg prot./ml, pH dependent (pH-optimum 7.1 to 7.4), temperature dependent with extremely low binding at 0-4 degrees C; the assay runs at 37 degrees C; it is ion dependent (Bmax:CaCl2 (5mM): + 100%; NaCl (5 mM): -50%); very sensitive to TRITON X-100 (Bmax at 0.01%; -70%); N-ethylmaleimide (0.5 mM): Competitive inhibition; no change in non-specific binding; there are no effects by puromycin plus GTP; VAL binds to synaptic membranes of human frontal cortex with KD-values several fold lower than that observed with homogenates, the distribution of VAL-binding is different in various human brain areas and can be inhibited by L-leucine, L-isoleucine, L-serine, DL-threonine, glycine and D-valine, while aromatic amino acids, beta-alanine, GABA, taurine, glutamate, proline and gamma-glutamyltaurine have no effects of 10(-3) M.

Aged↗
PubMed1983

Symptoms and side effects in the course of Parkinson's disease.

From our investigations, we are tempted to assume that all types of akinesia, including "freezing", off-phases, Yo-Yoing and akinetic crises, are primarily symptoms of PD, while hyperkinesia, stretch spasms and pharmacotoxic psychosis are "side-effects". Therefore side-effects can be triggered by antiparkinsonian therapy while they will disappear after withdrawal of the drugs inducing them. Antiparkinson drugs alleviate major symptoms like akinesia and rigidity but sometimes and especially as reflection of advanced parkinsonism, might amplify minor symptoms (freezing, off-phases, Yo-Yoing), which then predominantly at high drug doses occur earlier and more intensively. Therefore, minor symptoms can be observed more frequently in the advanced stages of PD. Depressed phases belong to the symptom complex as is bradyphrenia and dizziness. Bradyphrenia is the psychic correlate to akinesia. Dementia, if at all is a symptom, but more likely this disease occurs occasionally in combination with parkinsonism.

Autonomic Nervous System Diseases↗
PubMed1982

Excretion of biogenic amine metabolites in anorexia nervosa.

Urinary metabolites of catecholamines and indoleamines have been investigated in 16 patients with anorexia nervosa (AN) and 13 controls using a HPLC-method. Vanillic mandelic acid, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, 3,4-dihydroxyphenylacetic acid, 5-hydroxyindole acetic acid and indoleacetic acid were significantly decreased in the pre-treatment phase. In four patients long-term treatment including parenteral and enteral nutrition together with psychological methods resulted in an increase in the levels of these substances and this correlated with increased weight gain and urinary creatinine. It is concluded that both central and peripheral disturbances are involved in AN, particularly with regard to biogenic amine metabolism.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Morphological and biochemical changes in the aging brain: pathophysiological and possible therapeutic consequences.

Significant reduction in brain weight and in the number of cortical neurons with increase of astroglia in aging brain and SDAT are associated with decreased synthesis and turnover of some neurotransmitters, particularly affecting the DAergic system. Progressive loss of TH activity reaching in SDAT almost the low levels of Parkinson disease is associated with progressive decline in DA concentration in the nigro-striatal system. Increase in MAO-B activity and in the ratio of MAO-B: MAO-A reported by some authors in aging brain and SDAT, however, was not confirmed in human frontal cortex in both Parkinson disease and SDAT. However, the location of both types of MAO in human brain is debatable, since preliminary studies indicate that, unlike in rat brain, MAO-B appears to be the major degradating enzyme of biogenic amines in human brain, while MAO-A might be associated, at least in part, with neuronal structures. Reduction in DAergic parameters in aging brain are also reflected in a decrease of adenylate cyclase activity and of D2 DA receptors. Animal data on decrease of DA-receptor density in the striatum with age were confirmed in human Parkinson disease and Alzheimer disease. These disturbances in neuronal feedback systems may be responsible for pathophysiological and behavioral changes in old age.

Aged↗
PubMed1982

[Antagonism of the ammonia effect on serotonin receptors by L-valine].

Ammonia and valine influence the activity of serotonin receptors in membranes of frontal cortex taken from brain removed at postmortem: Ammonia reduces maximal binding capacity of serotonin receptors, and this effect can be antagonized by valine. This modulatory effect of valine seems to be efficient at a lower level in tissues of patients with hepatic coma. Branched chain amino acids may have efficient therapeutic effects in hepatic coma due firstly to effects on the blood brain barrier by a well known mechanism of action and secondly to molecular interaction at the synaptic membrane.

Aged↗
PubMed1981

The effects of lisuride and some other dopaminergic agonists on receptor binding in human brain.

The effect of lisuride, bromocriptine, CQ 32-084 and CU 32-085 on the specific binding of radiolabelled spiperone to homogenates of human putamen taken post-mortem has been investigated. In addition, the binding of 3H-lisuride to such preparations has been studied. Lisuride is found to inhibit spiperone binding to the dopamine receptor at very low concentrations and to bind to the beta-adrenergic receptor at somewhat higher levels. Lisuride binding to the dopamine receptor was found to be antagonist-like. A measure of the in vivo effect of lisuride was obtained from investigations of brain tissue taken from a patient treated with the drug before death.

Brain↗
PubMed1981

Transitional states of central serotonin receptors in Parkinson's disease.

Crude membrane preparations from the frontal cortex of controls and parkinsonian patients were used to demonstrate affinity changes of the specific 3H-5-hydroxytryptamine (5-HT) binding sites. Two such sites were notable in controls, a finding consistent with earlier observations. In Parkinson's disease, both high- and low-affinity sites are significantly decreased. Additional experiments either with prolonged incubation times or pre-incubation with N-ethylmaleimide change the two affinities to a single high-affinity or low-affinity constant. The concept of transitional states of 5-HT receptors is discussed and seems to have important implications in the treatment of parkinsonism.

Aged↗
PubMed1981

Tranylcypromine isomers in the treatment of Parkinson's disease. Biochemical effects.

Isomers of the monoamine oxidase inhibitor tranylcypromine were administered separately to 15 hospitalized parkinsonian patients. The activity of the platelet enzyme, the plasma and urinary tranylcypromine, were measured. While the (+)isomer inhibited monoamine oxidase to a greater extent, both isomers increased plasma phenylethylamine. Differences between the pharmacokinetics of the two isomers were substantial, (-)tranylcypromine being excreted much faster.

Blood Platelets↗
PubMed1981

Tranylcypromine isomers and Parkinson's disease: new aspects of an old drug.

The tranylcypromine stereoisomers have been investigated in a series of comparative trials in Parkinsons' disease and the results indicate that doses below 3 mg/day, of the (+)-isomer in particular, are effective as adjuvant anti-parkinsonian therapy. Biochemical results, monitoring platelet monoamine oxidase (MAO) activity and plasma concentrations of drugs and phenylethylamine, an MAO substrate, showed such low doses of the (+)-isomer to inhibit MAO without inducing the hypertensive reaction sometimes observed at higher dosage. These findings, along with the observation of substantial pharmacokinetic differences between the two isomers are discussed, particularly in relation to reports on their efficacy in depressive illness.

Humans↗
PubMed1980

Progressive supranuclear palsy: clinico-pathological and biochemical studies.

Ten autopsy cases of Progressive Supranuclear Palsy (PSP) are reported. Age at onset ranged from 16 to 67 years and the duration of illness 3 to 24 years. The clinical features were aggressive mental retardation in 4 cases with early onset, paroxysmal dysequilibrium, ophthalmoplegia, rigidity and akinesia, pseudobulbar palsy and variable degrees of dementia. Neuropathology showed widespread neurofibrillary degeneration associated with system-bound neuronal loss and gliosis in subcortical areas, particularly affecting the subthalamic nucleus, substantia nigra, brainstem tegmentum and dentate nuclei, with no or little involvement of the cerebral cortex. The distribution of the lesions and the ultrastructure of the neurofibrillary tangles made of 15 nm straight filaments (seen in one case) in PSP are different from postencephalitic parkinsonism, Guam Parkinson-dementia complex and brainstem affection in (pre)senile dementia. Post-mortem biochemical analysis of two brains disclosed severe reduction of tyrosine hydroxylase, the key synthetic enzyme of the catecholamine pathway, not only in the nigrostriatal system as seen in Parkinson's disease, but in most areas of the brain-stem and limbic system. The implication and possible pathogenic and therapeutic significance of these biochemical findings are discussed. The etiology of PSP and its nosological position within the degenerative extrapyramidal disorders remain unknown.

Adolescent↗