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Previous Volume 346:2007-2008 June 20, 2002 Number 25 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: Seshadri and colleagues (Feb. 14 issue)¹ report that high homocysteine levels are a risk factor for Alzheimer's disease. The effect of homocysteine on brain tissue is influenced by the absence within this tissue of two of the major metabolic routes for the elimination of homocysteine: betaine-mediated conversion and transsulfuration.^2,3 Consequently, under conditions of folate deprivation, homocysteine can be eliminated only by export from the neuron. Increased export is problematic, however, as the authors point out, since homocysteine activates N-methyl-D-aspartate receptors and potentiates glutamate excitotoxicity.⁴ Minimizing homocysteine export may therefore be critical for nervous tissue, and it . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Thomas, P., Fenech, M. (2007). A review of genome mutation and Alzheimer's disease. Mutagenesis 22: 15-33 [Abstract] [Full Text]