Effects of Amino Acid Feedings in Schizophrenic Patients Treated with Iproniazid

Pollin, William; Cardon, Philippe V.; Kety, Seymour S.

doi:10.1126/science.133.3446.104

Cited by 330 publications

(72 citation statements)

References 9 publications

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“…The first evidence for a role of DNA methylation in schizophrenia came from the observation that treatment with an S-adenosyl-methionine precursor L-methionine, actually intensifies a number of schizophrenic symptoms (Pollin et al, 1961). Given that S-adenosyl-methionine is the methyl donor for the DNA methylation reaction, this result suggests that hypermethylation of DNA may contribute to schizophrenia.…”

Section: Dna Methylation In Schizophreniamentioning

confidence: 99%

“…A second psychiatric condition in which altered DNA methylation has long been implicated is schizophrenia (Pollin et al, 1961;Bredy et al, 2010). The first evidence for a role of DNA methylation in schizophrenia came from the observation that treatment with an S-adenosyl-methionine precursor L-methionine, actually intensifies a number of schizophrenic symptoms (Pollin et al, 1961).…”

Section: Dna Methylation In Schizophreniamentioning

confidence: 99%

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Epigenetic Treatments for Cognitive Impairments

Day

Sweatt

2011

Neuropsychopharmacol

109

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Epigenetic mechanisms integrate signals from diverse intracellular transduction cascades and in turn regulate genetic readout. Accumulating evidence has revealed that these mechanisms are critical components of ongoing physiology and function in the adult nervous system, and are essential for many cognitive processes, including learning and memory. Moreover, a number of psychiatric disorders and syndromes that involve cognitive impairments are associated with altered epigenetic function. In this review, we will examine how epigenetic mechanisms contribute to cognition, consider how changes in these mechanisms may lead to cognitive impairments in a range of disorders and discuss the potential utility of therapeutic treatments that target epigenetic machinery. Finally, we will comment on a number of caveats associated with interpreting epigenetic changes and using epigenetic treatments, and suggest future directions for research in this area that will expand our understanding of the epigenetic changes underlying cognitive disorders.

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Section: Dna Methylation In Schizophreniamentioning

confidence: 99%

Section: Dna Methylation In Schizophreniamentioning

confidence: 99%

Epigenetic Treatments for Cognitive Impairments

Day

Sweatt

2011

Neuropsychopharmacol

109

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“…These studies showed that treatment with high-daily doses of L-methionine resulted in exacerbation of schizophrenic symptoms. 9,10 In addition, as compared to controls the rate of whole body methylation was found to be decreased in patients with schizophrenia. 11,12 It was suggested that these findings might reflect an enzymatic defect or a failure of a control mechanism of the single-carbon cycle in schizophrenic patients.…”

Section: Introductionmentioning

confidence: 97%

Homocysteine, methylenetetrahydrofolate reductase and risk of schizophrenia: a meta-analysis

Muntjewerff¹,

et al. 2005

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Elevated plasma homocysteine concentration has been suggested as a risk factor for schizophrenia, but the results of epidemiological studies have been inconsistent. The most extensively studied genetic variant in the homocysteine metabolism is the 677C4T polymorphism in the methylenetetrahydrofolate reductase (MTHFR) gene, resulting in reduced enzyme activity and, subsequently, in elevated homocysteine. A meta-analysis of eight retrospective studies (812 cases and 2113 control subjects) was carried out to examine the association between homocysteine and schizophrenia. In addition, a meta-analysis of 10 studies (2265 cases and 2721 control subjects) on the homozygous (TT) genotype of the MTHFR 677C4T polymorphism was carried out to assess if this association is causal. A 5 lmol/l higher homocysteine level was associated with a 70% (95% confidence interval, CI: 27-129) higher risk of schizophrenia. The TT genotype was associated with a 36% (95% CI: 7-72) higher risk of schizophrenia compared to the CC genotype. The performed meta-analyses showed no evidence of publication bias or excessive influence attributable to any given study. In conclusion, our study provides evidence for an association of homocysteine with schizophrenia. The elevated risk of schizophrenia associated with the homozygous genotype of the MTHFR 677C4T polymorphism provides support for causality between a disturbed homocysteine metabolism and risk of schizophrenia.

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“…Homocysteine may elicit DNA damage response in neurons that promotes apoptosis and hypersensitivity to excitotoxicity. An oral methionine load has classically been reported to exacerbate schizophrenia and is of course converted to homocysteine (104)(105)(106).…”

Section: Amino Acid Disturbances: Glycine Serine and Homocysteinementioning

confidence: 99%