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Stefan Bleich, MD; Helge Frieling, MD; Thomas Hillemacher, MD

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

We read with great interest the recent article by Brown et al¹ about the impact of prenatal elevated homocysteine levels on the risk of schizophrenia. The presented findings are striking and of high importance for a better understanding of the pathogenesis of schizophrenia.

The authors hypothesize that homocysteinemia may elevate the risk of schizophrenia via an action on the delivery of oxygen. This may be one possible and important explication to take into consideration. However, another important pathophysiological mechanism should be taken into account when discussing the presented findings. Homocysteine is known to act as a methyl-donator when activated to S-adenosyl-methionine and by this way influences global and gene promoter-specific DNA methylation.^2-3 There is mounting evidence that altered promoter DNA methylation could play a substantial role in mediating differential regulation of genes and in facilitating short-term adaptation in response to the . . . [Full Text of this Article]

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RELATED ARTICLE

Elevated Prenatal Homocysteine Levels as a Risk Factor for Schizophrenia
Alan S. Brown, Teodoro Bottiglieri, Catherine A. Schaefer, Charles P. Quesenberry, Jr, Liyan Liu, Michaeline Bresnahan, and Ezra S. Susser
Arch Gen Psychiatry. 2007;64(1):31-39.
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