A Clinical Trial with a New Anticonvulsant Drug, α-(P-Aminophenyl)-α-Ethyl Glutarimide Preparation 16038 (Ciba)

1959 ◽  
Vol 105 (439) ◽  
pp. 448-456 ◽  
Author(s):  
Walter Fabisch

Derivatives of glutarimide are known to exert an effect upon the central nervous system. To name only two which are widely used for clinical purposes: Glutethimide (“Doriden”) is a sedative, Bemigride (“Megimide”) a stimulant. Preparation 16038 (Ciba) α-(p-aminophenyl)-α-ethyl glutarimide, in animal experiments had shown properties which suggested its use as an anticonvulsant, and this paper is an account of a clinical trial with the substance on in- and out-patients suffering from epilepsy.

1956 ◽  
Vol 34 (11) ◽  
pp. 1557-1561 ◽  
Author(s):  
Stanley O. Winthrop ◽  
Stella Sybulski ◽  
Roger Gaudry ◽  
Gordon A. Grant

Basic derivatives of 6-chloroquinazoline and phthalazine have been synthesized and screened for their physiological action on the central nervous system. Sodium dialkylaminoalkoxides and the appropriate chlorobenzodiazine were brought together to yield basic ethers of 6-chloroquinazoline and phthalazine respectively. 1-(γ-Dimethylaminopropylamino)phthalazine was also prepared.


1982 ◽  
Vol 60 (5) ◽  
pp. 715-719 ◽  
Author(s):  
K. Ramabadran ◽  
C. Suaudeau ◽  
J. J. C. Jacob

The effects of N-methylnaloxone following subcutaneous and intracerebroventricular administrations on nociception were investigated using the hot plate technique. Unlike naloxone, subcutaneous administration of N-methylnaloxone did not enhance the nociceptive reactions. In contrast, intracerebroventricular injection of N-methylnaloxone produced antinociception and tremor. Compared with naloxone, N-methylnaloxone was very weak in precipitating the signs of abstinence in mice rendered acutely dependent on morphine. Two factors, poor penetration into the central nervous system and steric hindrance, might render N-methylnaloxone very weak and hence both these factors must be taken into consideration while analyzing the effects following quaternary derivatives of opioid antagonists.


2013 ◽  
Vol 154 (4) ◽  
pp. 128-135 ◽  
Author(s):  
György Csaba

The notion of the perinatal „hormonal imprinting” has been published at first in 1980 and since that time it spred expansively. The imprintig develops at the first encounter between the developing receptor and the target hormone – possibly by the alteration of the methylation pattern of DNA – and it is transmitted to the progeny generations of the cell. This is needed for the complete development of the receptor’s binding capacity. However, molecules similar to the target hormone (hormone-analogues, drugs, chemicals, environmental pollutants) can also bind to the developing receptor, causing faulty imprinting with life-long consequences. This can promote pathological conditions. Later it was cleared that in other critical periods such as puberty, imprinting also can be provoked, even in any age in differentiating cells. The central nervous system (brain) also can be mistakenly imprinted, which durably influences the dopaminergic, serotonergic and noradrenergic system and this can be manifested – in animal experiments – in alterations of the sexual and social behavior. In our modern age the faulty hormonal imprintig is inavoidable because of the mass of medicaments, chemicals, the presence of hormone-like materials (e.g. soya phytosteroids) in the food, and environmental pollutants. The author especially emphasizes the danger of oxytocin, as a perinatal imprinter, as it is used very broadly and can basically influence the emotional and social spheres and the appearance of certain diseases such as auitism, schizophrenia and parkinsonism. The danger of perinatal imprinters is growing, considering their effects on the human evolution. Orv. Hetil., 2013, 154, 128–135.


1971 ◽  
Vol 123 (1) ◽  
pp. 69-74 ◽  
Author(s):  
G. S. Baldwin ◽  
P. R. Carnegie

Two methylated derivatives of arginine were isolated from the encephalitogenic protein of myelin from the central nervous system. Evidence is presented for the proposed structures, ω-NN′-dimethylarginine and ω-N-monomethylarginine. In the encephalitogenic protein from human brain the proportion 1:6:10 for arginine:monomethylarginine:dimethylarginine residues was found to occur at position 107. Possible roles for the methylated arginine in conformational changes and altered ion-exchange behaviour are discussed.


2018 ◽  
Vol 13 (3-4) ◽  
pp. 70-75
Author(s):  
M.V. Khaitovych

Relevance. Anti-depressant effects of NMDA receptor antagonists have been proven, a close association between low levels of magnesium in the blood and depression. Therefore, in recent years, antidepressant properties of magnesium are actively studied in animal experiments. Objective: To review modern literary sources about the role of magnesium deficiency in the pathogenesis of diseases of the central nervous system. Materials and methods. Searching for a depth of 12 years at Scopus, Google Scholar. Results. The results of experimental and clinical researches pointed out on association between low level of magnesium in hair, liquor, brain with higher risk of development dementia, depression and anxiety. An additional supplementation with magnesium in patients associates with decreasing risk of ischemic stroke and dementia, in pregnancy – provides neuroprotection of fetus, in case of depression increases effectiveness of antidepressants, in brain injury associates with faster recovery of cognitive functions, in migraines - with decreasing in the frequency of attacks and improvement of the quality patients’ lives, in case of neuroleptic therapy - with the possibility of delayed appearance or absence of manifestations of drug parkinsonism. These changes are explained by antagonistic effects of magnesium on glutamate receptors, decreasing oxidative stress intensity as well as neural cell  apoptosis. Conclusion. Magnesium plays an important neuroprotective role.


2007 ◽  
Vol 504 (5) ◽  
pp. 550-569 ◽  
Author(s):  
Angeliki Louvi ◽  
Michio Yoshida ◽  
Elizabeth A. Grove

2021 ◽  
Vol 14 (11) ◽  
pp. 1156
Author(s):  
Viktoria Gudi ◽  
Nora Schäfer ◽  
Stefan Gingele ◽  
Martin Stangel ◽  
Thomas Skripuletz

Inflammatory attacks and demyelination in the central nervous system (CNS) are the key factors responsible for the damage of neurons in multiple sclerosis (MS). Remyelination is the natural regenerating process after demyelination that also provides neuroprotection but is often incomplete or fails in MS. Currently available therapeutics are affecting the immune system, but there is no substance that might enhance remyelination. Cytidine-S-diphosphate choline (CDP-choline), a precursor of the biomembrane component phospholipid phosphatidylcholine was shown to improve remyelination in two animal models of demyelination. However, the doses used in previous animal studies were high (500 mg/kg), and it is not clear if lower doses, which could be applied in human trials, might exert the same beneficial effect on remyelination. The aim of this study was to confirm previous results and to determine the potential regenerative effects of lower doses of CDP-choline (100 and 50 mg/kg). The effects of CDP-choline were investigated in the toxic cuprizone-induced mouse model of de- and remyelination. We found that even low doses of CDP-choline effectively enhanced early remyelination. The beneficial effects on myelin regeneration were accompanied by higher numbers of oligodendrocytes. In conclusion, CDP-choline could become a promising regenerative substance for patients with multiple sclerosis and should be tested in a clinical trial.


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