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 postulated disturbance of cyclic AMP (cAMP) in manic-depressive illness was investigated by using plasma as the biological material. Cyclic AMP was measured by a protein-binding assay, which was found very satisfactory for the purpose of this study. In the drug-free state, depressed patients (n = 28) had significantly lower and manic patients (n = 9) significantly higher plasma concentrations of cAMP than controls. Unmedicated manic-depressive subjects had normal cAMP levels during normothymic phases (n = 7). Cyclic AMP was reduced by neuroleptics in mania and elevated by tricyclics in depression. Lithium exerted a normalizing effect on cAMP in both phases of the illness. It is concluded that manic-depressive illness is associated with a disturbance in the cAMP system. The use of plasma rather than urine for the investigation of the state of cAMP in psychiatric disorders is advocated.
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PMID:Plasma cyclic AMP in manic-depressive illness. 20 68

The beta-adrenergic receptors were studied in vitro in lymphocytes obtained from patients with major affective disorders and controls. Specific L-[3H]-dihydroalprenolol binding was decreased in both depressed and manic patients compared to controls and euthymic patients. Isoproterenol-stimulated, but not prostaglandin El-stimulated, cyclic adenosine-3',5'-monophosphate production was decreased in manic and depressed patients. These results suggest decreased lymphocyte beta-receptor functioning in depression and mania. This decrease may be an index of changes in brain beta-receptors in mania and depression, or may simply reflect homeostatic regulation of peripheral beta-receptors in response to stress-induced increases in circulating catecholamines.
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PMID:Changes in lymphocyte beta-adrenergic receptors in depression and mania. 23 57

Onset of mania was evaluated retrospectively in 48 bipolar manic-depressive patients. Mania occurred as the initial episode in 40% of cases. In patients with initial episode of depression, approximately 80% developed mania prior to their third episodes of depression and within 5 years from the onset of this illness. Differences in type of illness onset were related to family history of bipolar illness and sex of the proband. Male patients with a positive family history were significantly more likely to manifest mania at onset of illness.
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PMID:Onset of mania in bipolar manic-depressive patients. 28 68

In order to evaluate the presumed involvement of altered noradrenergic receptor sensitivity in the switch process from depression into mania, we explored the relationship between pretreatment 3-methoxy-4-hydroxy-phenylglycol (MHPG) and tricyclic-induced mania or hypomania in bipolar depressed patients. Within the group of patients developing mania or hypomania on tricyclics, there was a strong positive correlation between pretreatment 24-hour urinary MHPG and the latency of onset of the episode. This finding is consistent with both the reported differences in MHPG excretion between unipolar and bipolar patients and the postulated noradrenergic involvement in the switch process.
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PMID:Tricyclic-induced mania and MHPG excretion. 29 43

The synaptic membrane protein D2 was measured in the cerebrospinal fluid (CSF) of manic-melancholic patients. The concentration of D2 increased with the age of the patients until about 35 years of age. No difference was found between the D2-concentration in CSF from a control group compared with different manic-melancholic subgroups. The D2-concentration in CSF collected from the patients during depression or mania was compared with CSF collected from the same patients when their moods were normalized. In the case of the depressed patients, we found that the D2-concentration increased slightly when the mood was normalized.
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PMID:Synaptic membrane protein D2 in the cerebrospinal fluid of manic-melancholic patients. 33 74

Seven men and one woman with primary affective disorder, mania, were given a slow intravenous infusion of physostigmine salicylate. In six patients, mood and thought content changed from mania toward depression as evaluated by either a visual analog mood scale or the Pettersen scale. Two other patients, who were the only predominantly irritable manics in the study, demonstrated little change in their hostility, although one became somewhat depressed. These findings are consistent with earlier reports of suppression of manic symptoms after physostigmine infusion in some but not all patients with mania. The pharmacologic mechanism of physostigmine reversal of manic symptoms may be the direct result of increased cholinergic activity or a result of the effect of increased cholinergic activity on other brain neurotransmitters.
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PMID:Physostigmine in mania. 33 69

Lithium carbonate has established itself as an effective therapeutic agent in primary affective disorders. As not all the patients with primary affective disorders respond to lithium therapy, it is necessary to identify responders prior to treatment. The important indicators of favourable lithium response include a definitive diagnosis of primary affective disorder, occurrence of less than four episodes of mania and depression within one year, psychotic features during both manic as well as depressive episodes, "grandiose-elated" picture during manic episodes; a family history of bipolar illness and response of affected family members to lithium treatment. While those with more than four episodes are not likely to respond to lithium therapy, those with episodes less frequent than once a year or two may not need prophylactic lithium. Among the depressed, hypersomnic depressed patients respond to lithium combined with a monoamine oxidase inhibitor. In addition to clinical predictors of response to lithium treatment, there are a number of pharmacokinetic, neurophysiological and biochemical indices which have been employed as supplementary predictors of response to lithium therapy.
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PMID:Prediction of lithium response in affective disorders. 34 5

In the last 20 years, the treatment of mood disorders has advanced immeasurably. We now have relatively safe and effective agents for the treatment of depression and mania. This review discusses two types of agents that elevate mood--tricyclic antidepressants and monoamine oxidase inhibitors--including the indications for their use and their modes of action, pharmacokinetics, side effects, and drug interactions.
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PMID:Series on pharmacology in practice: 1. Drugs that alter mood. I. Tricyclic agents and monoamine oxidase inhibitors. 37 90

Psychiatric research has made remarkable advances in understanding the pathophysiology of depressive illnesses. Biologic depressions are now understood as neurotransmitter deficiency diseases. Certain forms of depression are treated with tricyclic antidepressant drugs, which increase the amount of available neurotransmitters. Complicating the clinical picture, however, is the problem of wide variability of levels of tricyclic drugs in the plasma of persons receiving the same dosage. Another problem is the apparent linear dose-response relationship of imipramine hydrochloride and its sister compound desipramine hydrochloride while amitriptyline and nortriptyline follow an inverted U-shaped dose-response curve. However, with newer, more sophisticated diagnostic methods, combined with monitoring of tricyclic drug levels in plasma, therapeutic efficacy can approach 90 percent. Available neurotransmitters also can be increased using monoamine oxidase (MAO) inhibitors. Although MAO inhibitors have been less popular than the tricyclic drugs, recent clinical research tends to support their efficacy. Distinct individual differences in the rate of metabolism of MAO inhibitors have been found. New methods are being devised to detect these differences and monitor directly the effects of these drugs. One of these methods, platelet MAO inhibition, shows some clinical promise. Tricyclic drugs and MAO inhibitors have recently been joined by lithium carbonate, which shows notable efficacy in removing acute manic-depressive symptoms as well as preventing their return during maintenance treatment. Its utility in treating cyclic depressions without mania is now being explored by researchers.
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PMID:Recent advances in antidepressant drug treatment. 39 Aug 88

Efforts were made to develop an animal model for studies of the role of biogenic amines in a group of human "mood" diseases including mania and depression. Subadult, male olive baboons (Papio anubis), both normal and psychologically disturbed individuals, were anesthetized and administered 18O-enriched air for 60-130 minutes. Afterwards blood, urine, and cerebrospinal fluid were collected every hour, for 10 hours. The samples were subsequently fragmentographically analyzed for labelled metabolites of serotonin, dopamine, and norepinephrine. The results showed that significant incorporation of 18O was found in all metabolities studied, with a peak after about 4 hours. The effect of chlorpromazine injection on 18o-incorporation was also measured. It was found that chlorpromazine caused a faster rise in labelling and indicated the stimulation of dopamine turnover in the brain. The usefulness of the animal model and the in vivo labelling technique for biogenic amine determination in the brain was demonstrated by the fact that the technique was subsequently used in human patients with neurologic disease.
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PMID:The olive babbon (Papio anubis) as an animal model for research in affective disorders of man. 41 3


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