Research on DMAE

Eur J Med Res. 2003 May 30;8(5):183-91.

Efficacy of dimethylaminoethanol (DMAE) containing vitamin-mineral drug combination on EEG patterns in the presence of different emotional states.

Dimpfel W, Wedekind W, Keplinger I.

Pro Science, Private Research Clinic GmbH - med. Forschung und Entwicklung -, Kurt-Schumacher-Str. 9, D-35440 Linden, Germany. w.dimpfel@mewicon.at

The psychophysiological model of provoking different emotional states by watching film excerpts with various emotional contents was used to characterize drug action in 80 subjects (male/female=50%) with threshold emotional disturbance within a randomized, group-parallel, double-blind, placebo-controlled study. Analyzing the brain's electrical reaction during presentation of 5 videoclips of 7 min duration followed by 3 minutes pause revealed a content specific representation of topographical frequency changes. This procedure was repeated after 6 and 12 weeks of daily intake of a vitamin-mineral drug combination containing dimethylaminoethanol (DMAE) (Vitagerin Geistlich N) or placebo. Subjects taking the active drug for 3 months developed significant less theta and alpha1 power in sensomotoric areas of the cortex. The grade of change and statistical significance was dependend on the content of the excerpt, but the pattern of changes in general remained the same. Since decreases in theta and alpha1 electrical power have been associated with increased vigilance and attention, subjects taking the drug combination obviously were more active and felt better. - Analysis of the emotional change in mood profile as induced by the TV session was achieved by completing two different quenstionaires (POMS and Bf-S). Both scores revealed a better mood for the active drug group thus corroborating the results from EEG analysis. Therefore the vitamine-mineral drug combination containing DMAE can be interpreted to induce a psychophysiological state of better feeling of wellbeing on both levels of analysis mood and electrical pattern of brain activity in subjects suffering from borderline emotional disturbance.

PMID: 12844472 [PubMed - in process]

J Pharmacol Exp Ther. 1990 Jan;252(1):154-8.

Effect of dimethylaminoethanol, an inhibitor of betaine production, on the disposition of choline in the rat kidney.

Lohr J, Acara M.

Department of Medicine, Veteran's Administration Medical Center, Buffalo, New York.

The choline metabolite betaine has been shown to be an important organic osmoregulatory solute in the kidney. The isolated perfused rat kidney and kidney slice incubations were used to investigate the effect of 2-dimethylaminoethanol (DMAE), a choline oxidase inhibitor, on the renal excretion and metabolism of choline. In the isolated perfused kidney, [14C]choline, at an initial perfusate concentration of 300 microM, was effectively removed from the perfusate over 25 min, with nearly all the 14C in the perfusate accounted for by betaine during the remainder of the 90-min perfusion. DMAE at concentrations of 3.0 or 5.0 mM significantly decreased the rate of removal of [14C]choline from the perfusate and the rate of addition of [14C]betaine to the perfusate, yet [14C]betaine remained the only metabolite of choline in perfusate and urine. In kidney tissue slice experiments, conversion of [14C]choline to [14C]betaine was found in cortical, outer medullary and inner medullary regions of rat kidney. DMAE at 5.0 mM significantly inhibited [14C]betaine production in each of the three regions studied. These data show that DMAE is an effective inhibitor of betaine production by the kidney and, as such, may be an important agent for the study of osmoregulation by the kidney.

PMID: 2405150 [PubMed - indexed for MEDLINE]

Med Hypotheses. 1988 Aug;26(4):255-7.

Use of DMAE (2-dimethylaminoethanol) in the induction of lucid dreams.

Sergio W.

A food supplement, namely DMAE, that facilitates the induction of lucid dreams is discussed. Included is a brief consideration of the therapeutic potential of such dreams.

PMID: 3173167 [PubMed - indexed for MEDLINE]

Biochem Pharmacol. 1986 Aug 15;35(16):2693-702.

Effects of cerebro-protective agents on enzyme activities of rat primary glial cultures and rat cerebral cortex.

Bielenberg GW, Hayn C, Krieglstein J.

The effects of different cerebro-protective agents on selected key enzymes of the energy metabolism of rat primary glial cultures and rat cerebral cortex were studied. As indicators for the capacity of the most important pathways of energy metabolism the following enzyme activities were determined: hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK), lactate dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G-6-P-DH), malate dehydrogenase (MDH), glutamate dehydrogenase (GDH), and cytochrome-c-reductase (CCR). After a one week growth period, rat glial cultures were incubated for 3 or 4 weeks with the substances to be tested. Bencyclane (5 X 10(-5) mol/l) increased the activities of HK, G-6-P-DH, and LDH, whereas PFK and CCR were reduced. Pyritinol (10(-4) mol/l) led to a higher G-6-P-DH activity, simultaneously lowering the values for PFK, CCR, PK, LDH, and MDH. Under the influence of an extract of the leaves of Ginkgo bilobae (EGB; 100 mg/l) PFK, LDH, and MDH activities were reduced. All these alterations in enzyme activities went along with simultaneous reductions in protein content, therefore not allowing to exclude toxic effects with regard to the doses used. Moreover, direct interference with the analytical procedure was demonstrable for bencyclane and EGB. Piracetam (10(-3) mol/l), flunarizine (10(-6) mol/l), dihydroergocristine (5 X 10(-6) mol/l), and nicergoline (5 X 10(-6) mol/l) failed to induce any alteration in the employed doses. The most striking effects were obtained with meclofenoxate which was tested at 10(-3) and 10(-4) mol/l. The higher dose caused an elevation of HK, PFK, CCR, G-6-P-DH, GDH and MDH activities, while slightly reducing PK. With the lower dose of meclofenoxate CCR and G-6-P-DH activities were increased. Short-term incubation of the cultures with 10(-3) mol/l meclofenoxate for 24 hr led to an increase in LDH, G-6-P-DH, and GDH activities. Chronic incubation with meclofenoxate (10(-3) mol/l) followed by 48 hr deprivation of the drug resulted in elevated HK, PFK, CCR, G-6-P-DH, GDH, and MDH activities. These changes were accompanied by alterations in related metabolite levels. These include elevations in the concentration of creatine phosphate and fructose-1,6-bisphosphate, whereas glucose-6-phosphate levels were reduced. After one week of meclofenoxate deprivation the activities of CCR and G-6-P-DH were still elevated. The metabolites of meclofenoxate dimethylaminoethanol (DMAE; 10(-3) mol/l) and p-chlorophenoxyacetic acid (10(-3) mol/l) were also investigated.(ABSTRACT TRUNCATED AT 400 WORDS)

PMID: 2943286 [PubMed - indexed for MEDLINE]

Biomed Biochim Acta. 1986;45(8):1075-82.

Effects of nootropic drugs on some behavioural and biochemical changes after early postnatal hypoxia in the rat.

Gramatte T, Wustmann C, Schmidt J, Fischer HD.

Piracetam (PIR) and dimethylaminoethanol (DMAE) were tested with respect to their ability to prevent changes of the locomotor behaviour and of the dopamine release from striatum slices after an intermittent postnatal hypoxia in the rat (2nd-10th day of postnatal life). The drugs given to pregnant rats (from 12th day of gestation) and continued after delivery to the newborns (till 10th day of postnatal life) displayed antihypoxic effects. Perinatal DMAE- but not PIR-treatment diminishes the consequences of postnatal oxygen deprivation regarding the motor activity as well as the dopamine release of adult animals. Hypoxia-caused open field hyperactivity of developing rats was found to be reduced to control values in PIR-treated rats. Only minor effects were seen after DMAE-treatment, but a marked depressant own effect on the explorative activity was detectable.

PMID: 3778435 [PubMed - indexed for MEDLINE]

Exp Aging Res. 1978 Apr;4(2):133-9.

Effects of PCA and DMAE on the namatode Caenorhabditis briggsae.

Zuckerman BM, Barrett KA.

Concentration of 6.8 mM DMAE did not retard age pigment accumulation in Caenorhabditis briggsae. However, when the nematodes were exposed to 6.8 mM PCA + 6.8 mM DMAE combined, the accumulation of age pigment was significantly retarded. A combination of 3.4 mM DMAE + 3.4 mM PCA had no effect on age pigment. It is concluded from this study that PCA and DMAE act in concert to produce the observed effect on age pigment. In respect to this parameter neither molecule was effective alone. The results indicate that the effect of centrophenoxine on age pigment might be enhanced by retarding the hydrolysis of centrophenoxine. The accumulation of electron dense aggregates, thought to be aggregates of cross-linked molecules, was reduced by 6.8 PCA + 6.8 DMAE. It is suggested that centrophenoxine be tested for its ability to remove random, unwanted cross-linkages in higher animals.

PMID: 348477 [PubMed - indexed for MEDLINE]

J Gerontol. 1977 Jan;32(1):38-45.

Effects of dimethylaminoethanol upon life-span and behavior of aged Japanese quail.

Cherkin A, Exkardt MJ.

The lysosome hypothesis of aging predicts that membrane stabilizers will extend life-span. Stabilizers containing the dimethylaminoethanol moiety (DMAE) have been reported to extend the life-span of drosophila and mice. We tested the prediction in Japanese quail (N = 15) by administering DMAE bitartrate (18.4 mg/kg/day) in the drinking water for 69 weeks, starting at 195 weeks of age. A matched control group (N = 14) received tartaric acid (4.0 mg/kg/day) in the water. Contrary to the prediction, the DMAE-treated group has a shorter life-span after start of treatment (49 weeks) than the controls (69 weeks). No significant differences between the groups were observed in body weight or daily fluid intake. Three behavioral studies were carried out on survivors at 243-249 weeks of age, namely; activity response to light-flash; sexual mounting response to a female quail; and classical conditioning of the heart rate. Aged quail differed from young-adults in changes in motor activity in response to light flashes. Aged quail appeared less responsive initially to reinforced conditioning trials and demonstrated extinction when light flash was not followed by electric shock. There were no detectable differences in latency to mount or in basal heart rate, either as a function of age or as a function of DMAE treatment.

PMID: 830732 [PubMed - indexed for MEDLINE]

J Am Geriatr Soc. 1977 Jun;25(6):241-4.

Senile dementia: treatment with deanol.

Ferris SH, Sathananthan G, Gershon S, Clark C.

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.

PMID: 864168 [PubMed - indexed for MEDLINE]

Clin Pharmacol Ther. 1975 May;17(5):534-40.

Deanol and methylphenidate in minimal brain dysfunction.

Lewis JA, Young R.

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.

PMID: 1092513 [PubMed - indexed for MEDLINE]