Effects of the novel antidepressant S-adenosyl-methionine on α1- and β-adrenoceptors in rat brain

Cohen, Bruce M.; Stramentinoli, G.; Sosa, Ana Luisa; Babb, Suzann M.; Olgiati, Vincenzo R.

doi:10.1016/0014-2999(89)90540-2

Cited by 17 publications

(4 citation statements)

References 46 publications

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“…In rodents, SAMe dose-dependently decreases immobility time in the forced swimming test (22) and increases concentrations of CNS monoamine neurotransmitters, serotonin and norepinephrine (23). Animal studies show that chronic SAMe administration increases dopaminergic tone in brain regions, including rat striatum (24), and increases CNS beta-adrenergic receptor density and activity (25,26). Thus, studies of central monoaminergic neurotransmitters support proposed mechanisms for SAMe antidepressant effects.…”

Section: Resultsmentioning

confidence: 99%

“…Since SAMe is the methyl donor in this reaction, its levels become depleted with L-dopa treatment. Pre-clinical studies show that acute treatment with L-dopa markedly depletes SAMe levels in liver and brain tissue (25). In PD, L-dopa treatment is associated with increased levels of total homocysteine in plasma (89) and CSF (90), as a by-product of increased COMT methylation of L-dopa.…”

Section: Resultsmentioning

confidence: 99%

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<em>S</em>-Adenosylmethionine (SAMe) for Neuropsychiatric Disorders

Sharma¹,

Gerbarg²,

Bottiglieri³

et al. 2017

J. Clin. Psychiatry

122

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Objective A systematic review on S-adenosylmethionine (SAMe) for treatment of neuropsychiatric conditions and co-morbid medical conditions. Data Sources Searches were conducted between 7/15/2015 and 9/28/2016 by combining search terms for SAMe (s-adenosyl methionine or s-adenosyl-l-methionine) with terms for relevant disease states including (major depressive disorder, MDD, depression, perinatal depression, human immunodeficiency virus, HIV, Parkinson's, Alzheimer's, dementia, anxiety, Schizophrenia, psychotic, 22q11.2, substance abuse, fibromyalgia, osteoarthritis, hepatitis, or cirrhosis). Additional studies were identified from prior literature. Ongoing clinical trials were identified through clinical trial registries. Study Selection Of the 174 records retrieved, 21 were excluded, as they were not original investigations. An additional 21 records were excluded, for falling outside of the scope of this review. Of the 132 studies included in this review, 115 were clinical trials and 17 were preclinical studies. Data Extraction A wide range of studies was included in this review in order to capture information that would be of interest to psychiatrists in clinical practice. Results This review of SAMe in the treatment of major depressive disorder found promising but limited evidence of efficacy and safety to support the use of SAMe as a monotherapy and as an augmentation for other antidepressants. Additionally, preliminary evidence suggests that SAMe may ameliorate symptoms in certain neurocognitive, substance use and psychotic disorders and co-morbid medical conditions. Conclusions SAMe holds promise as a treatment for multiple neuropsychiatric conditions, but the body of evidence has limitations. The encouraging findings support further study of SAMe in both psychiatric and co-morbid medical illnesses.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

<em>S</em>-Adenosylmethionine (SAMe) for Neuropsychiatric Disorders

Sharma¹,

Gerbarg²,

Bottiglieri³

et al. 2017

J. Clin. Psychiatry

122

View full text Add to dashboard Cite

show abstract

“…[5][6][7] Exogenous SAMe has a low bioavailability due to first-pass effects, rapid metabolism, chemical instability of the molecule, and past problems with tablet dissolution in some commercial preparations. 5,8,11 An enteric-coated formulation is in widespread use, which reaches a peak plasma level within 5 hours and has a half-life of 1-2 hours.…”

mentioning

confidence: 99%

Bioavailability and Lack of Toxicity of S‐Adenosyl‐l‐Methionine (SAMe) in Humans

Gören¹,

Stoll²,

Damico³

et al. 2004

Pharmacotherapy

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“…The changes in membranes may lead to changes in receptor function. Chronic treatment of rats with SAM causes alterations in brain adrenergic binding sites, but the changes seen are different from those that occur with the majority of other antidepressant treatments (Cohen et al 1989). Neuroendocrine studies with humans suggest that SAM increases dopaminergic function (Fava et al 1990).…”

Section: Folic Acid Dejciency and S-adenosylmethioninementioning

confidence: 95%

The 1989 Borden Award Lecture. Some effects of dietary components (amino acids, carbohydrate, folic acid) on brain serotonin synthesis, mood, and behavior

Young

1991

Can. J. Physiol. Pharmacol.

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This review covers three areas in which dietary components may influence brain serotonin synthesis, mood, and behavior. In the first, tryptophan-deficient amino acid mixtures have been used to lower brain tryptophan and serotonin in normal human subjects for experimental purposes. Results suggest that low serotonin can cause lowered mood and increased aggression, but that it is probably not involved in any simple way in carbohydrate craving. Low serotonin levels can block the analgesic effect of morphine in humans. The second area concerns deficiencies of folic acid, which can cause low brain serotonin and lowered mood. Folate supplements may be useful in some depressed patients. The third area concerns the effect of carbohydrate meals. Although it is well established that carbohydrate meals raise brain tryptophan and serotonin in the rat, and that protein meals lower them, any effects of carbohydrate or protein meals on human brain serotonin are likely to be negligible under most circumstances. Carbohydrate meals can have definite effects on mood and behavior in humans, and there are a variety of mechanisms, other than alterations in brain serotonin, that might mediate these effects.

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Effects of the novel antidepressant S-adenosyl-methionine on α1- and β-adrenoceptors in rat brain

Cited by 17 publications

References 46 publications

<em>S</em>-Adenosylmethionine (SAMe) for Neuropsychiatric Disorders

<em>S</em>-Adenosylmethionine (SAMe) for Neuropsychiatric Disorders

Bioavailability and Lack of Toxicity of S‐Adenosyl‐l‐Methionine (SAMe) in Humans

The 1989 Borden Award Lecture. Some effects of dietary components (amino acids, carbohydrate, folic acid) on brain serotonin synthesis, mood, and behavior

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