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)

Folate (vitamin B9) plays a crucial role in fundamental cellular processes, including nucleic acid biosynthesis, methyl group biogenesis and amino acid metabolism. The detection and correction of folate deficiency prevents megaloblastic anaemia and reduces the risk of neural tube defects. Coexisting deficiencies of folate and vitamin B12 are associated with cognitive decline, depression and neuropathy. Folate deficiency and excess has also been implicated in some cancers. Excessive exposure to folic acid, a synthetic compound used in supplements and fortified foods, has also been linked to adverse health effects. Of at least three distinct laboratory markers of folate status, it is the total abundance of folate in serum/plasma that is used by the majority of laboratories. The analysis of folate in red cells is also commonly performed. Since the folate content of red cells is fixed during erythropoiesis, this marker is indicative of folate status over the preceding ~4 months. Poor stability, variation in polyglutamate chain length and unreliable extraction from red cells are factors that make the analysis of folate challenging. The clinical use of measuring specific folate species has also been explored. 5-Methyltetrahydrofolate, the main form of folate found in blood, is essential for the vitamin B12-dependent methionine synthase mediated remethylation of homocysteine to methionine. As such, homocysteine measurement reflects cellular folate and vitamin B12 use. When interpreting homocysteine results, age, sex and pregnancy, specific reference ranges should be applied. The evaluation of folate status using combined markers of abundance and cellular use has been adopted by some laboratories. In the presence of discordance between laboratory results and strong clinical features of deficiency, treatment should not be delayed. High folate status should be followed up with the assessment of vitamin B12 status, a review of previous results and reassessment of folic acid supplementation regime.
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PMID:Laboratory assessment of folate (vitamin B9) status. 3022 13

Folate deficiency has been suggested as a risk factor for depression in preclinical and clinical studies. Several hypotheses of mechanisms underlying folate deficiency-induced depressive symptoms have been proposed, but the detailed mechanisms are still unclear. In this study, we assessed whether post-weaning folate deficiency affect neurological and psychological function. The low folate diet-fed mice showed depression-like behavior in the forced swim test. In contrast, spontaneous locomotor activity, social behavior, coordinated motor skills, anxiety-like behavior and spatial memory did not differ between control and low folate diet-fed mice. In the dentate gyrus (DG) of the hippocampus, decreased number of newborn mature neurons and increased number of immature neurons were observed in low folate diet-fed mice. Staining with Golgi-Cox method revealed that dendritic complexity, spine density and the number of mature spines of neurons were markedly reduced in the DG of low folate diet-fed mice. Stress response of neurons indicated as c-Fos expression was also reduced in the DG of low folate diet-fed mice. These results suggest that reduction in the degree of maturation of newborn hippocampal neurons underlies folate deficiency-induced depressive symptoms.
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PMID:Post-weaning folate deficiency induces a depression-like state via neuronal immaturity of the dentate gyrus in mice. 3217 64

Major depressive disorder is most commonly treated with a combination of medication and psychotherapy. For those people that do not benefit from the standard therapy or prefer non-pharmacologic therapy, folate supplementation may be an option. Folate is normally acquired through the diet and folate deficiency is associated with depression. In the brain, folate is one nutrient among others involved in the production of the neurotransmitters that affect mood. Studies involving folate supplementation for the treatment of depression have had mixed results but have omitted to take into account the genetic polymorphisms, such as the ones in methyltetrahydrofolate reductase (MTHFR), that affect folate metabolism. Supplementation with L-methylfolate may overcome the folate metabolism problems seen in individuals with disadvantageous genetic polymorphisms.
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PMID:The Role of Folate and MTHFR Polymorphisms in the Treatment of Depression. 3282 2


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