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At least 19 recordsLinked to original sources

PubMed1977

Is 2-dimethylaminoethanol (deanol) indeed a precursor of brain acetylcholine? A gas chromatographic evaluation.

Acute administration of deanol-p-acetamidobenzoate (Deaner; deanol) has been reported to elevate brain choline (CH) and acetylcholine (ACh) levels. We have developed a specific and sensitive gas chromatographic assay to measure deanol levels in tissue and have applied this assay to our studies of the effect of acute deanol administration on deanol, ACh and Ch levels in rodent brains. Details of the method are described in this text. This procedure is quantitative and yields reproducible results over a wide range of deanol concentrations (0.30-200 nmol). Seven endogenous and pharmacological parameters have been studied using this procedure. In control rodent brain, liver, heart, lung and plasma, we detected no free endogenous deanol (less than 1 nmol/g). After deanol administration, we were able to detect deanol in tissue and have attempted to determine a relationship between these levels and values of ACh in the same tissue. Regardless of deanol pretreatment time (1-30 minutes) or doses (33.3-3000 mg/kg i.p.) used, we detected no increase in mouse whole brain ACh levels. Likewise, there was no detectable elevation in ACh levels in rat whole brain, cortex, striatum or hippocampus after a 15-minute pretreatment with 550 mg/kg of deanol (i.p.). The only elevation in ACh levels which we detected occurred selectively in the striatum of mice pretreated with a massive dose (900 mg/kg i.p.) of deanol for 30 minutes. This selective increase in striatal ACh levels oculd not, however, be related to levels of deanol in the striatum because there was no greater accumulation of deanol in the striatum than in other brain areas tested or in whole brain. These data do not confirm the results of other investigators who reported elevations in whole brain or striatal ACh levels after acute administration of lower doses of deanol. The data emphasize the need for further investigation into the mode of action of deanol and question its suggested role as an immediate precursor of ACh synthesis in the central nervous system.

Acetylcholine↗

PubMed1981

Behavioral effects of deanol, of hemicholinium and of their interaction.

The present experiments were designed to study behavioral effects of two chemicals, which have opposite influences on the cholinergic neurotransmitter system, and of their interaction. It has been proposed that deanol is a direct precursor of acetylcholine (ACh) in brain and may enhance cholinergic transmission, while hemicholinium-3 (HC-3) acts to decrease ACh synthesis. Rats served as subjects. Doses of the drugs were based on results of earlier experiments; all were injected cerebroventricularly. The six treatment groups were: saline only; HC-3 (10 micrograms); HC-3 (10 micrograms) + deanol (1 microgram); HC-3 (10 micrograms) + deanol (10 micrograms); deanol (1 microgram); and deanol (10 micrograms). Behaviors measured were: reactivity to visual and tactile stimuli; resistance to capture and handling, vocalization, muscular tension; reactivity to non-contingent aversive stimulation; and, shock-induced defence reaction. With the exception of the defence reaction, all behaviors showed significant effects between the various drug treatments: deanol had no significant effect on the behaviors; animals receiving HC-3 only clearly showed responses which were enhanced above the levels of any of the other treatment groups; deanol had a dose-dependent effect of suppressing HC-3 enhanced behavior. The present results are consistent with the generalization that decreased cholinergic activity is associated with hyper-reactivity, and increased cholinergic activity with hyporeactivity. They indicate that the behavioral effects of deanol are dependent upon the state of the cholinergic system, interacting in combination with HC-3 but not alone.

Animals↗

PubMed1978

Deanol acetamidobenzoate inhibits the blood-brain barrier transport of choline.

Competition by deanol (dimethylaminoethanol) with choline for uptake from the bloodstream into the brain was demonstrated by simultaneous intracarotid administration of carbon 14-labeled choline with deanol (plus tritiated water and indium 113m, to calculate a brain uptake index) and by measuring the brain uptake of 14C-labeled choline mixed with sera from rats pretreated with deanol (300 or 500 mg/kg 8 or 30 minutes earlier). The inhibition constant for inhibition of choline uptake by deanol (159 micrograms) was actually lower than the Michaelis constant for choline itself (442 micrograms); hence, the affinity of the carrier mechanism for deanol is at least as great as it is for choline. Deanol administration also elevated blood choline levels; thus, the effect of the drug on brain choline (and acetylcholine) levels is the result of the increase it produces in blood choline and the suppression it causes in choline uptake. These findings may explain discrepant results from laboratories seeking increases in brain acetylcholine or clinical improvement in patients with tardive dyskinesia after deanol treatment.

Acetylcholine↗

PubMed1979

Dimethylaminoethanol (deanol) metabolism in rat brain and its effect on acetylcholine synthesis.

Specific methods utilizing combined gas chromatography mass spectrometry were used to measure the metabolism of [2H6] deanol and its effects on acetylcholine concentration in vitro and in vivo. In vitro [2H6]deanol was rapidly taken up by rat brain synaptosomes, but was neither methylated nor acetylated. [2H6]Deanol was a weak competitive inhibitor of the high affinity transport of [2H4]choline, thus reducing the synthesis of [2H4]acetylcholine. In vivo [2H6]deanol was present in the brain after i.p. or p.o. administration, but was not methylated or acetylated. Treatment of rats with [2H6]deanol significantly increased the concentration of choline in the plasma and brain but did not alter the concentration of acetylcholine in the brain. Treatment of rats with atropine (to stimulate acetylcholine turnover) or with hemicholinium-3 (to inhibit the high affinity transport of choline) did not reveal any effect of [2H6]deanol on acetylcholine synthesis in vivo. However, since [2H6]deanol did increase brain choline, it may prove therapeutically useful when the production of choline is reduced or when the utilization of choline for the synthesis of acetylcholine is impaired.

Acetylcholine↗

PubMed1977

Deanol acetamidobenzoate (Deaner) in tardive dyskinesia.

A total of twenty-nine patients have thus far been treated with deanol in various dosage levels for periods ranging from five to thirty days. Clinical response has been pronounced, even dramatic, in seven patients, moderate but significant in nine patients, and slight to insignificant in thirteen others. Videotape rating and quantitative accelerometry, to the extent that they constitute novel and stress-inducing experiences may not be representative of global clinical changes. Deanol did not produce the anticipated elevation in choline levels postulated to be one mechanism of its action. The failure of deanol to achieve this effect may most probably be attributed to interval after last dose, to inadequate level of deanol or to some alteration in choline metabolism in the presence of deanol. The etiology of tardive dyskinesia at biochemical and structural levels is complex. For some patients improvement has been dramatic and clearly associated with deanol. Others appear to exhibit minimal response which cannot be differentiated from placebo or environmental effects. Our present strategy, in common with that of other authors includes the administration of a "challenge" dose of rapid acting injectable cholinomimetic agents (e.g. physostigmine) and dopamine-blocking agents (e.g. haloperidol) with placebo controls. In this manner therapy may be more rationally selected for long-term use and may logically include deanol. The correlation of such predictive challenges with response to long-term treatment is an area for much more well controlled study.

Choline↗

PubMed1975

Deanol and methylphenidate in minimal brain dysfunction.

Deanol, a putative acetylcholine precursor, has been used as a treatment for childhood hyperactivity for years. Efficacy has not been satisfactorily established, however. Seventy-four children referred for problems with learning, including many with hyperactivity, were screened for neurological or psychiatric illness, then given deanol, methylphenidate, or placebo in a double-blind fashion for 3 months. Maintenance dose for methylphenidate was 40 mg daily; for deanol, 500 mg. Behavior rating forms, reaction time, and a series of standard psychometric tests were given before and after treatment. Both drugs showed significant improvement on a number of tests; the pattern and degree of change differed slightly for the two. In this paradigm, deanol thus appeared to improve performance in children with learning and behavior disorders. The mechanism of action remains speculative; proof that deanol increases acetylcholine is scanty, and there is a theoretical basis for actually assuming an anticholinergic effect. Further clinical studies on deanol are indicated.

Analysis of Variance↗

PubMed1981

Deanol affects choline metabolism in peripheral tissues of mice.

Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors.

Animals↗

PubMed1979

Ineffectiveness of deanol in tardive dyskinesia: a placebo controlled study.

In a double-blind placebo-controlled study, deanol acetamidobenzoate, administered in doses up to 1.5 g q.d. for three weeks to chronic schizophrenic patients presenting moderate to severe tardive dyskinesia, failed to alleviate the dyskinetic movements. However, there was a tendency for a significant increase in the schizophrenic symptoms of the deanol-treated group relative to the control group. The ineffectiveness of deanol in alleviating tardive dyskinesia is consistent with its inability to enhance brain acetylcholine synthesis. The worsening of the schizophrenic symptoms may possibly result from an interference by deanol with central cholinergic function.

Adult↗

PubMed1978

Deanol and physostigmine in the treatment of L-dopa-induced dyskinesias.

Deanol and placebo were administered to 10 parkinsonian patients with levodopa-induced dyskinesias in a double-blind, crossover fashion. Deanol and placebo did not differ significantly in their effects on dyskinesias. The reported properties of deanol seem to be attributable to a placebo effect. There was no correlation with the results of the physostigmine test. Despite these disappointing results deanol remains intriguing, because in individual cases remarkable improvements on dyskinesias are reported.

Aged↗

PubMed1975

Deanol in the treatment of levodopa-induced dyskinesias.

Levodopa-induced dyskinesias frequently limit the clinical efficacy of levodopa therapy in Parkinson's disease. Deanol recently has been reported to be of value in relieving the dyskinesias by acting through a central cholinergic mechanism. Seventeen outpatients with levodopa-induced dyskinesias were given deanol in dosages of 300 to 900 mg per day. The dyskinesias improved in four of the patients, remained unchanged in five, and worsened in eight. In all four patients who showed improvement after institution of deanol therapy, the improvement continued after the patients were switched to a placebo. One of these patients also demonstrated improvement in his parkinsonism, while two others experienced a worsening in their parkinsonism. Deanol does not appear to be effective in the treatment of levodopa-induced dyskinesias.

Aged↗

PubMed1981

Double blind controlled trial of deanol in tardive dyskinesia.

Thirty three chronic psychiatric hospital subjects with oral tardive dyskinesia were divided into three groups. The subjects were matched for severity of symptoms then randomly assigned to treatment with a placebo, 1 g deanol or 2 g deanol per day. Statistical analysis showed that after 30 days treatment, there was a significant reduction in the mean rating of the movements of the group of 11 subjects on 2 g deanol per day. Six of these subjects showed substantial reduction in movement. Further studies using this dosage of deanol are unwarranted.

Aged↗

PubMed1977

Deanol in Gilles de la Tourette Syndrome: a preliminary investigation.

On the basis of its pharmacologic action Deanol (dimethyl aminoethanol) was hypothesized to be of benefit in the Gilles de la Tourette Syndrome. In one case report the addition of Deanol to perphenazine did not result in an improvement of uncontrollable movements or involuntary speech utterances. Gilles de la Tourette Syndrome is a condition combining organic and psychogenic features existing in the interface between two etiologies. Classically the disease begins in childhood and is characterized by the appearance of sudden involuntary movements, involuntary speech utterances frequently consisting of curse words (coprolalia), and imitative phenomena such as echolalia and echopraxia. Neurotic symptomatology such as anxiety and obsessive thinking have also been reported. This condition is regarded neuropharmacologically as a dopaminergic state that responds to drugs with antidopaminergic activity e.g. the phenothiazines and butyrophenones. Deanol (dimethyl aminoethanol) is a putative cholinergic agonist and has reported effectiveness in conditions where there is a predominance of dopaminergic versus cholinergic activity, e.g. levodopa-induced dyskinesias, neuroleptic induced tardive dyskinesia, and Huntington's chorea. Because of its effectiveness in dopaminergic states it was hypothesized that Deanol could also be of benefit in the Gilles de la Tourette Syndrome.

Adult↗

PubMed1977

Deanol in the treatment of tardive dyskinesia.

Ten hospitalized chronic psychotic patients with symptoms of tardive dyskinesia were given deanol and placebo, each for 8 weeks following a double-bline, crossover design. No psychotropic agents were administered during the trial. Improvement occurred in all patients during the first treatment phase regardless of which drug the patients received; seven patients were on deanol and three on placebo during this time. The possible reasons for this decrease were discussed. It was concluded that deanol may have contributed to the decline but that its effect on the disorder was not dramatic.

Aged↗

PubMed1977

Senile dementia: treatment with deanol.

Recent research indicates a possible cholinergic involvement in memory processes and thus the possibility that acetylcholine deficiency may underlie memory impairment in senile dementia. Deanol (2-dimethylaminoethanol), which is assumed to increase brain acetylcholine, was given openly for 4 weeks to 14 senile outpatients, to determine the safety of the drug and whether or not it reduces cognitive impairment. The dosage was gradually increased to 600 mg three times daily during the first two weeks, with no adverse effects. Ten patients improved globally and 4 were unchanged (p less than .01). The total score on the Sandoz Clinical Assessment-Geriatric (SCAG) was lowered by the third week (p less than .01), primarily as a result of reduced depression, irritability and anxiety, and increased motivation-initiative. However, neither the clinical ratings nor an extensive pre- versus post-treatment series of cognitive tests revealed changes in memory or other cognitive functions. Since a similar separate study with a different compound produced no behavioral changes, it is unlikely that the improvement with deanol was due entirely to placebo effects. The results thus suggest that although deanol may not improve memory, it may produce positive behavioral changes in some senile patients.

Aged↗

PubMed1978

Deanol, lithium and placebo in the treatment of tardive dyskinesia. A double-blind crossover study.

A double-blind crossover study on the effects of deanol and lithium carbonate was conducted on a sample of 29 chronic schizophrenic patients with tardive dyskinesia. In addition to his usual treatment with different neuroleptics, each patient received during an 8-week period either deanol, lithium carbonate or placebo. A 4-week wash-out period was inserted between each of the 8-week periods of experimental treatment of the tardive dyskinesia. The administration of either deanol, lithium carbonate or placebo added to the neuroleptic treatment did not produce a statistically significant improvement of tardive dyskinesia in our patient population as a whole. Favorable and unfavorable responses are discussed.

Adult↗

PubMed1975

The effects of dimethylaminoethanol (deanol) on cerebral cortical neurons.

2-Dimethylaminoethanol and acetylcholine were iontophoretically tested on deep, spontaneously firing, neurons of the rat cerebral cortex. All identified corticospinal cells and 71% of the unidentified ones were excited by Deanol. Eight percent of the latter group were inhibited. All but one neuron responded similarly to ACh and Deanol, when both substances were tested on the same neuron. Atropine reversibly blocked these responses. The implications of these observations are discussed with regard to cholinergic synapses in the brain and the rationalization of the therapeutic use of Deanol.

Acetylcholine↗

PubMed1980

[Treatment with dimethylaminoethanol (deanol) in neuroleptic induced tardive dyskinesia].

A double blind cross-over study of 20 patients wiht tardive dyskinesia due to chronic use of neuroleptics showed no difference between efficacity of Deanol (Deaner) and placebo. Several patients improved with Deanol (Deaner), whereas several other patients showed increasing dyskinesia. The same phenomenon could be observed in the placebo group. Tolerance of the compound was very good. Results of an additional open study however suggest that the administration of Deanol (Deaner) may be tried as long as no other means are available to define those patients who will react favorably to this medication.

Adult↗

PubMed1977

Deanol acetamidobenzoate treatment in choreiform movement disorders.

Deanol acetamidobenzoate was administered in double-blind, crossover fashion with placebo to five patients with tardive dyskinesia, three patients with Huntington's chorea, and one patient with posthemiplegic chorea. No significant effect on dyskinesia was observed. Preliminary administration of physostigmine salicylate to patients with tardive dyskinesia had a variable effect, while benztropine mesylate produced no change. Since the status of deanol as an effective precursor of acetylcholine is uncertain, further trials with putative cholinergic agents remain warranted in choreiform syndromes.

Benztropine↗