понедельник, 16 августа 2010 г.

S-Аденозилметионин при депрессии

The actions of S-adenosyl methionine in the central nervous system have been reviewed previously (3, 7, 8). SAMe acts as a major methyl donor for the synthesis of brain amines and maintenance of phospholipid cell membranes. Low levels of SAMe have been reported in the cerebrospinal fluid (CSF) of severely depressed patients. Oral and parenteral administration of SAMe result in a rise in CSF SAMe concentrations, indicating the compound crosses the blood-brain barrier. An increase in SAMe levels has been positively correlated with improvement in depression. SAMe concentrations also appear to rise in patients who respond to other antidepressants such as desipramine. SAMe is produced in the one-carbon cycle involving folate, homocysteine, and vitamin B12 and abnormalities of each of these compounds has been associated with depression. In short, the hypothesis is that abnormalities in the one-carbon cycle may result in low concentrations of SAMe that in turn may limit the synthesis of brain neurotransmitters such as serotonin, norepinephrine, and dopamine. This may directly contribute to depressive symptoms or interfere with or limit the action of other antidepressants. Administration of SAMe may ameliorate these deficiencies or augment antidepressants and facilitate neurotransmission.

In this issue, Papakostas and colleagues (1) report the results of an adjunctive trial of S-adenosyl methionine (SAMe) in 73 patients with major depression who had failed a prior selective serotonin reuptake inhibitor trial at an adequate dose for at least 6 weeks. Patients were randomly assigned to SAMe, with a targeted dose of 800 mg twice a day, or placebo. Both were added to the ongoing antidepressant regimen and continued for 6 weeks. Response according to the primary outcome, the Hamilton Depression Rating Scale (HDRS), was more likely with SAMe (36.1%) than with placebo (17.6%), as was remission (HDRS score ≤ 7): 25.8% versus 11.7%, respectively. Differences were statistically significant and clinically meaningful.

S-Adenosyl Methionine (SAMe) Augmentation in Major Depressive Disorder

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