ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1994.tb05402.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Introduction‐ S‐adenosyl‐l‐methionine (SAMe) is a naturally‐occurring substance which is a major source of methyl groups in the brain.Material and methods‐ We conducted a meta‐analysis of the studies on SAMe to assess the efficacy of this compound in the treatment of depression compared with placebo and standard tricyclic antidepressants.Results‐ Our meta‐analysis showed a greater response rate with SAMe when compared with placebo, with a global effect size ranging from 17% to 38% depending on the definition of response, and an antidepressant effect comparable with that of standard tricyclic antidepressants.Conclusion‐ The efficacy of SAMein treating depressive syndromes and disorders is superior with that of placebo and comparable to that of standard tricyclic antidepressants. Since SAMe is a naturally occurring compound with relatively few side‐effects, it is a potentially important tre

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1994.tb05403.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Introduction‐ The relationship between plasma levels of S‐adenosylmethionine (SAMe), an endogenous methyl donor, and clinical response were studied in patients with a DSM‐III‐R diagnosis of major depression.Material and methods‐ A double‐blind randomized protocol comparingoral SAMe with oral desipramine, involving a total of 26 patients, was employed.Results‐At the end of the 4‐week trial, 62% of the patients treated with SAMe and 50% of the patients treated with desipramine had significantly improved. Regardless of the type of treatment, patients witha 50% decrease in their Hamilton Depression Scale (HAM‐D) score showed a significant increase in plasma SAMe concentration.Conclusion‐ The significant correlation between plasma SAMe levels and the degree of clinical improvement in depressed patients regardless of the type of treatment suggests that SAMe may play an important role

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1994.tb05404.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Introduction‐ S‐adenosylmethionine (SAMe) is an important methyl donor in over 35 methylation reactions involving DNA, proteins, phosphalipids and catechol‐ and indole‐ amines.Material and Methods‐ This article reviews the studies that have examined brain and blood levels of SAMe in several psychological, neurological and metabolic disorders.Results‐ Although studies have found no consistent changes in whole blood SAMe levels in psychiatric patients, other investigators have found low cerebrospinal fluid (CSF) SAMe levels in patients with neurological disorders such as Alzheimer's dementia, subacute combined degeneration of the spinal cord (SACD), and HIV‐related neuropathies, as well as in patients with metabolic disorders such as 5, 10‐CH2‐H4 folate reductase deficiency.Conclusion‐ Intravenous or oral administration of SAMe thus represents a possible treatment for these neurological and

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1994.tb05405.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Introduction‐ Central nervous system (CNS) methyltransferases methylate a wide range of substrates including proteins, lipids, nucleic acids and hormones. In every instance the methyl donor is S‐adenosylmethionine (SAMe) and the demethylated product is S‐adenosylhomocysteine (SAH).Methylation can be disrupted when there is an inadequate supply of methionine synthase (following vitamin B12deficiency or folate deficiency), SAMe synthetase (due to ethanol), or SAH hydrolase (for unknown reasons).Material and Methods5‐week‐old pigs were maintained in an environment of either air or nitrous oxide, which inhibits methionine synthase, and were fed eithera methionine‐unsupplemented or methionineenriched diet. After 3 to 10 weeks, pigs were killed by pentabarbitone injection and the levels of methionine and SAMe in the pigs' brain, spinal cord, plasma, liver, and kidney assessed.Results‐ Pigs maintained in nitrous oxide displayed a dramatic fall in methionine levels in plasma and brain tissues but maintained relatively normal SAMe levels in these tissues. Brain and spinal cord cystathionine levels were markedly elevated, especially in those animals receiving oral methionine, as in the absence of methionine synthase homocysteine can be metabolized only through the catabolic pathway to cystathionine and cysteine.Conclusion‐ Disorders such as vitamin B12deficiency or folate deficiency inhibit methylation by limiting the availability of SAMe or by elevating levels of the inhibitor SAH. In either case, the disruption of a wide range of methylation reactions can cause clinical sequelae ranging from structural abnormalities such as myelopathy to functional abnormalities suc

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1994.tb05406.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Introduction‐ Axon growth and axon regeneration are complex processes requiring an adequate supply of certain metabolic precursors and nutrients.Material and methods‐ This article reviews the studies examining some of the processes of protein modification fundamental to both nerve regeneration and to the continuous and adequate supply of specific factors such as arginine, S‐adenosylmethionine and polyamines.Results‐ The process of arginylation notably increases following nerve injury and during subsequent regeneration of the nerve, with the most likelyfunction of arginine‐modification of nerve proteins being the degradation of proteins damaged through injury. It appears that defective methyl group metabolism may be one of the leading causes of demyelination, as suggested by the observation of reduced cerebrospinal fluid concentrations of s‐adenosylmethionine (SAMe) and 5‐methyltetrahydrofolate, the key metabolites in methylation processes, in patients with a reduction in myelination of corticospinal tracts. Polyamine synthesis, which depends strongly on the availability of both SAMe and arginine, markedly increases in neurons soon after an injury. This “polyamine‐response” has been found to be essential for the survival ofthe parent neurons after injury to their axons. Polyamines probably exert their effects through involvement in DNA, RNA and protein synthesis, or through post‐translational modifications that areindicated as the most relevant events of the “axon reaction.”Conclusions‐ Nerve regeneration requires the presence of arginine, s‐adenosylmethionine, and polyamines. Further studies are needed to explore the mechanism

ISSN:0001-6314    

DOI:10.1111/j.1600-0404.1994.tb05407.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY