Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible effects on psychomotor performance, concentration, attention, and mood of acamprosate (calciumacetylhomotaurinate) were assessed using a randomized, double-blind, cross-over, placebo-controlled design involving 12 healthy male volunteers. Acamprosate 2 g daily per os or placebo was administered for seven days and separated by washout intervals of at least 21 days. Objective tests evaluated psychomotor functions (simple reaction time measurement, binary choice reaction test, computerized visual searching task, sustained attention test). Mood was assessed using the Beck Depression Inventory and the Beschwerde-Liste to assess subjective physical impairment. Additionally, a visual 3-D illusion paradigm was applied to measure the psychotomimetic effect. A dose of acamprosate of 2 g/day for seven days was free of any significant effects on mood, concentration, attention, psychomotor performance and did not produce any subjective sedation, excitation or psychotomimetic effects.
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PMID:Lack of psychotomimetic or impairing effects on psychomotor performance of acamprosate. 965 38

The objective of this study was to compare acamprosate with placebo in the treatment of alcohol-dependent patients during a 6-month post-detoxification treatment and a 3-month medication-free follow-up. Patients (n = 330) were detoxified and randomized to treatment with acamprosate (1998 mg/day) or placebo within an out-patient programme including medical counselling, psychotherapy and self-help groups. The main outcome criterion was drinking behaviour as assessed by: abstinence/relapse ratio, cumulative abstinence duration (CAD) and the period of continued abstinence. Anxiety, depression and craving were also monitored. Intention to treat (ITT) statistical principles were followed. Twenty-five per cent of patients dropped out over the first 6 months. At the end of the treatment period, the abstinence rate was 57.9% for acamprosate and 45.2% for placebo (P = 0.03). The CAD was 110+/-77 days for acamprosate and 89+/-77 days for placebo (P = 0.016). Patients on acamprosate had a higher continuous abstinence rate and experienced less severe relapses. No differential effect was noted for anxiety, depression or craving. Treatment remained positive, but not significant, 3 months after termination of study medication. No significant difference in adverse events was noted between treatment groups. Acamprosate treatment over 180 days was consistently more effective than placebo to maintain abstinence and to diminish relapse severity.
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PMID:Acamprosate and relapse prevention in the treatment of alcohol dependence: a placebo-controlled study. 1078 98

Over the last 20 years, the role of adjuvant pharmacotherapy in optimising outcome in rehabilitation programmes for alcohol-dependent patients has become increasingly evident. New avenues for rational drug treatment have arisen from better understanding of the neurobiological substrates of alcohol dependence, including adaptive changes in amino acid neurotransmitter systems, stimulation of dopamine and opioid peptide systems, and, possibly, changes in serotonergic activity. Disulfiram, naltrexone and acamprosate are currently the only treatments approved for the management of alcohol dependence. However, there is still no unequivocal evidence from randomised controlled clinical trials that disulfiram improves abstinence rates over the long term. Aversive therapy with disulfiram is not without risk for certain patients, and should be closely supervised. Both naltrexone and acamprosate improve outcome in rehabilitation of alcohol-dependent patients, but seem to act on different aspects of drinking pathology. Naltrexone is thought to decrease relapse to heavy drinking by attenuating the rewarding effects of alcohol. However, data from the naltrexone clinical trial programme are somewhat inconsistent, with several large studies being negative. Acamprosate is believed to maintain abstinence by blocking the negative craving that alcohol-dependent patients experience in the absence of alcohol. The clinical development programme has involved a large number of patients and studies, of which the vast majority have shown a beneficial effect of acamprosate on increasing abstinence rates. Both drugs are generally well tolerated; nausea is reported by around 10% of patients treated with naltrexone, while the most frequent adverse effect reported with acamprosate is diarrhoea. Another opioid receptor antagonist, nalmefene, has shown promising activity in pilot studies, and may have a similar profile to naltrexone. Data from studies of SSRIs in alcohol dependence are somewhat heterogeneous, but it appears that these drugs may indirectly improve outcome by treating underlying depression rather than affecting drinking behaviour per se. Similarly, the anxiolytic buspirone may act by ameliorating underlying psychiatric pathology. Dopaminergic neuroleptics, benzodiazepines and antimanic drugs have not yet demonstrated evidence of activity in large controlled clinical trials. Trials with drugs acting at serotonin receptors have yielded disappointing results, with the possible exception of ondansetron. Because the biological basis of alcohol dependence appears to be multifactorial, the future of management of alcoholism may be combination therapy, using drugs acting on different neuronal pathways, such as acamprosate and naltrexone. Pharmacotherapy should be used in association with appropriate psychosocial support and specific treatment provided for any underlying psychiatric comorbidities.
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PMID:Pharmacotherapy of alcohol dependence: a review of the clinical data. 1518 19

The effect of drug for alcoholism treatment acamprosate (campral) on spontaneous electrical activity of frontal cortical neurons was studied in rats. Acamprosate after acute intraperitoneal administration (600 mg/kg) and microiontophoretic application reduced the frequency of spike activity in about 30 % of cells studied. The agent didn't change the magnitude and form of action potentials. Microiontophoretically applied acamprosate reduced the excitatory responses to ethanol electroosmotically applied to neurons at "small doses" (ejected current < 50 nA) and increased the value of neuronal depression induced by ethanol at the "large doses" (ejected current 50 nA). Effects of acamprosate were dose independent. It is suggested that acamprosate has no interaction with specific postsynaptic receptors and its action is determined by presynaptic mechanisms.
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PMID:[Electrophysiological study of acamprosate effects on frontal cortical neurons in rats]. 2400 80