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Oberdoerffer P, Michan S, McVay M, Mostoslavsky R, Vann J, Park SK, Hartlerode A, Stegmuller J, Hafner A, Loerch P, Wright SM, Mills KD, Bonni A, Yankner BA, Scully R, Prolla TA, Alt FW, Sinclair DA.
SIRT1 redistribution on chromatin promotes genomic stability but alters gene expression during aging. Cell.
2008 Nov 28;135(5):907-18.
PubMed Abstract
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Related News: DC: Developing But Debatable—Deacetylase Inhibitors for CNS Disease?
Comment by: Sigfrido Scarpa
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Submitted 15 December 2008
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Posted 16 December 2008
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Deacetylation is a wide and complex epigenetic mechanism, which could involve undesired targets. The use of specific compounds to obtain epigenetic silencing of genes in AD treatment is much more preferable and safe. We published several papers in which we show the involvement of gene methylation in AD pathology. References: Fuso A, Nicolia V, Cavallaro RA, Ricceri L, D'Anselmi F, Coluccia P, Calamandrei G, Scarpa S. B-vitamin deprivation induces hyperhomocysteinemia and brain S-adenosylhomocysteine, depletes brain S-adenosylmethionine, and enhances PS1 and BACE expression and amyloid-beta deposition in mice. Mol Cell Neurosci. 2008 Apr;37(4):731-46. Abstract
Cavallaro RA, Fuso A, D'Anselmi F, Seminara L, Scarpa S. The effect of S-adenosylmethionine on CNS gene expression studied by cDNA microarray analysis. J Alzheimers Dis. 2006 Aug;9(4):415-9. Abstract
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