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)

Subacute combined degeneration of the spinal cord is a rare neurologic complication of folate deficiency. Progressive gait disturbance, weakness, confusion, and depression developed in a 39-year-old man. He had taken phenobarbital for more than 2 years. He was bedbound, with new loss of position and vibration senses in the lower extremities. His hemoglobin was 2.9/dl, mean corpuscular volume 122 fl, vitamin B12 428 pg/ml, and folate 1 ng/ml. Peripheral blood and bone marrow showed megaloblastic anemia. Serum methylmalonic acid and homocysteine levels were consistent with folate deficiency, not B12 deficiency. Treatment with folate and packed erythrocytes resulted at 4 months in overall improvement, including walking. Position sense was restored, and vibration sense had become nearly normal. The authors found no cause for folate deficiency except phenobarbital.
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PMID:Case report: subacute combined degeneration of the spinal cord from folate deficiency. 748 26

This review focuses on the biochemical and clinical aspects of methylation in neuropsychiatric disorders and the clinical potential of their treatment with ademetionine (S-adenosylmethionine; SAMe). SAMe is required in numerous transmethylation reactions involving nucleic acids, proteins, phospholipids, amines and other neurotransmitters. The synthesis of SAMe is intimately linked with folate and vitamin B12 (cyanocobalamin) metabolism, and deficiencies of both these vitamins have been found to reduce CNS SAMe concentrations. Both folate and vitamin B12 deficiency may cause similar neurological and psychiatric disturbances including depression, dementia, myelopathy and peripheral neuropathy. SAMe has a variety of pharmacological effects in the CNS, especially on monoamine neurotransmitter metabolism and receptor systems. SAMe has antidepressant properties, and preliminary studies indicate that it may improve cognitive function in patients with dementia. Treatment with methyl donors (betaine, methionine and SAMe) is associated with remyelination in patients with inborn errors of folate and C-1 (one-carbon) metabolism. These studies support a current theory that impaired methylation may occur by different mechanisms in several neurological and psychiatric disorders.
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PMID:The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. 752 20

To test the hypothesis that cyanocobalamin (vitamin B12) is an effective treatment for winter seasonal affective disorder (SAD). 2 weeks of double-blind placebo washout, followed by random assignment to parallel treatments for 2 weeks with cyanocobalamin vs. placebo. Observations were made during weekly outpatient visits. All subjects met criteria for SAD. 27 patients were studied. After the washout period, 14 were randomly assigned to 1.5 mg cyanocobalamin (3 x/day) and 13 remained on placebo on the same schedule. 29 item SIGH-SAD scores were used to determine antidepressant efficacy. No significant differences were found in the responses between the two groups. Cyanocobalamin does not appear to be an effective short-term treatment for depression in SAD patients. The usefulness as a treatment for SAD of the methylated form of Vitamin B12, which has been used extensively in related studies, remains to be explored.
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PMID:A controlled trial of cyanocobalamin (vitamin B12) in the treatment of winter seasonal affective disorder. 785 61

Ninety-nine consecutive unmedicated outpatients with a major depressive illness had blood drawn for measurement of serum folate (SF), red cell folate (RCF), and vitamin B12 within 24 hours of completion of ratings of severity of depression at the beginning and ending of a 5-week trial of desmethylimipramine (mean dose = 149.2 mg/day, range = 75-225 mg). As compared with nonresponders, responders had a significantly higher mean SF at baseline (nonresponders = 13.8 nmol/l; responders = 17.7 nmol/l) and RCF showed a significant inverse correlation with severity of depression and a significant positive correlation with age of onset of illness. At week 5, change in severity of depression was significantly correlated with change in RCF, and significantly more responders than nonresponders had an increase in RCF. The possible role of folate status in the regulation of mood and response to treatment is discussed.
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PMID:Change in folate status with antidepressant treatment. 787 Aug 51

The pineal gland has been implicated recently in the pathogenesis of multiple sclerosis (MS), a chronic demyelinating disease of CNS. Since nocturnal melatonin secretion is low in some groups of patients with mental depression, we predicted lower melatonin secretion in MS patients with history of affective illness compared to those without psychiatric disorders. To test this hypothesis, we studied single nocturnal plasma melatonin levels and the incidence of pineal calcification (PC) on CT scan in a cohort of 25 MS patients (4 men, 21 women; mean age = 39.4 years, SD = 9.3), 15 of whom had a history of coexisting psychiatric disorders with predominant affective symptomatology. Other factors that may be related to depression such as vitamin B12, folic acid, zinc, magnesium, and homocysteine, were also included in the analysis. Neither any of the metabolic factors surveyed nor the incidence of PC distinguished the psychiatric from the control group. However, the mean melatonin level in the psychiatric patients was significantly lower than in the control group. Since low melatonin secretion in patients with depression may be related to a phase-advance of the circadian oscillator regulating the offset of melatonin secretion, we propose that the depression of MS likewise may reflect the presence of dampened circadian oscillators. Furthermore, since exacerbation of motor symptoms in MS patients may be temporally related to worsening of depression, we propose that circadian phase lability may also underlie the relapsing-remitting course of the disease. Consequently, pharmacological agents such as lithium or bright light therapy, which have been shown to phase-delay circadian rhythms, might be effective in the treatment of affective symptoms in MS as well as preventing motor exacerbation and hastening a remission from an acute attack.
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PMID:Nocturnal melatonin secretion in multiple sclerosis patients with affective disorders. 806 28

Changes in circulating and tissue concentrations of several vitamins have been reported in diabetic animals and human subjects. In this study, the effect of short-term (2 weeks) streptozotocin diabetes on folate, B6, B12, thiamin, nicotinate, pantothenate, riboflavin and biotin in liver, kidney, pancreas, heart, brain and skeletal muscle of rats was investigated. The tissue distribution of vitamins varied widely in normal rats. Diabetes significantly lowered folate in kidney, heart, brain, and muscle; B6 in brain; B12 in heart; thiamin in liver and heart; nicotinate in liver, kidney, heart and brain; pantothenate in all tissues; riboflavin in liver, kidney, heart, and muscle. These results indicate that experimental diabetes causes a depression of several water-soluble vitamins in various tissues of rats.
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PMID:Tissue concentrations of water-soluble vitamins in normal and diabetic rats. 840 64

In a chronic toxicity study in the rat, bidisomide administered as a dietary admixture produced a dose-related lowering of reticulocytes and leucocytes. Plasma alanine aminotransferase activity was increased at 300 mg/kg and decreased at 900 mg/kg. The potential mechanisms of these effects were investigated by comparing the responses in groups of male Sprague-Dawley rats receiving a control diet, or 300 or 1200 mg/kg/day bidisomide. Subsets of these groups were co-treated subcutaneously with folinic acid or with a vitamin B1, B6, B12 complex. Subsets of control and 300 mg/kg groups were maintained on a 20-25% feed restriction regimen for 3 months, to mimic the depression in body weight gain observed in animals receiving 1200 mg/kg. Body weight gains were significantly reduced at 1200 mg/kg and in all feed-restricted animals. Plasma and liver alanine aminotransferase (ALT) and plasma aspartate aminotransferase (AST) levels were also reduced at this dose level. At 300 mg/kg, plasma transaminases, glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SDH) activities were increased. These changes were prevented in animals receiving folinic acid supplementation. Plasma glucose, triglycerides, and unsaturated and total iron binding capacities were decreased, while plasma iron levels tended to increase, mainly at the high dose. Vitamin supplementation prevented a decrease in reticulocyte counts at 300 mg/kg. Bidisomide increased urinary formimino-glutamic acid (FIGLU) excretion but did not affect methylmalonic acid (MMA) or taurine excretion. The effect on FIGLU at 1200 mg/kg was prevented by folinic acid co-treatment. Absolute liver weight was lowered at both dose levels and in feed-restricted animals. However, the relative liver weights were unaffected. Thymidine kinase and thymidylate synthase activity of the bone marrow cells were not altered by the bidisomide treatment. Except for the increase in plasma transaminase, GLDH and SDH levels at 300 mg/kg, changes in clinical chemistry parameters are considered to result mainly from nutritional restrictions. Changes in hematologic parameters appear to be related to the combination of decreased feed consumption (leukocytes) and decreased availability or utilization of folates (reticulocytes). This alteration, however, did not affect DNA synthesis in bone marrow. The prevention by folinic acid, but not by feed restriction, of the elevation of liver enzymes at 300 mg/kg is an intriguing, yet unexplained finding. There was no evidence that bidisomide affected B6 and B12 availability.
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PMID:Effect of folate supplementation on clinical chemistry and hematologic changes related to bidisomide administration in the rat. 858 20

Utilization of dietary protein in vitamin B12 (B12)-deficient rats was evaluated by determinating the content of plasma protein, urinary excretion of nitrogen compounds, and nitrogen-balance after the rats were fed on a B12-deficient soy bean protein diet by pair-feeding for 100 days. The severe B12-deficiency was confirmed in rats by a remarkable increase in urinary methylmalonic acid excretion and a remarkable decrease in the hepatic B12 level. Growth of B12-deficient rats was significantly retarded as compared both with ad libitum-feeding control rats and pair-feeding control rats. The growth retardation due to B12-deficiency was alleviated by the administration of 1 microgram/day of CN-B12 for 30 days. Plasma total protein and albumin levels in rats fed on a B12-deficient diet decreased, compared with those in pair-feeding control, and increase in urea-nitrogen was observed. The excretion of urinary nitrogen compounds, such as urea-nitrogen, allantoin, and creatinine, was significantly depressed by B12-deficiency compared with those in pair-feeding control. The administration of CN-B12 to B12-deficient rats for 30 days resulted in the recovery of the changes in plasma proteins and urinary excretion of nitrogen compounds. The above results suggested that the extreme B12-deficiency depressed the utilization of dietary protein in rats. Moreover, the decrease in urinary urea-nitrogen excretion was supposed to be due to the adaptation by the depression of the dietary protein utilization.
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PMID:Utilization of dietary protein in the vitamin B12-deficient rats. 878 21

We investigated the effect of theophylline administration on circulating vitamin levels in children with asthma. Twenty-three asthmatic children, ranging in age from 7 to 15 with a mean of 10.8 years and including 16 patients who were treated with slow-release theophylline and 7 patients not receiving any type of theophylline preparation, were enrolled in this study. They all were inpatients who had been hospitalized for the control of asthma. Steady-state serum theophylline and vitamin A, B1, B2, B6, B12 and C levels were evaluated in these patients. Circulating vitamin B1 and B6 levels were depressed in asthmatic children treated with theophylline compared to those not receiving the agent (38.4 +/- 1.6 (mean +/- SEM) vs. 46.4 +/- 3.5 ng/ml and 7.1 +/- 0.5 vs. 11.8 +/- 2.1 ng/ml, respectively, p < 0.05). A significant negative correlation between theophylline and circulating levels of vitamin B6 was demonstrated in the subjects of this study (rs = -0.657, p < 0.001). In contrast, no relationship was noted between theophylline and circulating vitamin B1 levels. Theophylline did not affect circulating vitamin A, B2, B12 or C levels. We conclude that theophylline induces depression of circulating vitamin B1 and B6 levels in asthmatic children, although a dose-dependent interaction between theophylline and vitamin B1 would be unlikely.
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PMID:Relation between theophylline and circulating vitamin levels in children with asthma. 903 3

Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
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PMID:Electroencephalography as a diagnostic tool in dementia. 906 24


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