Citicoline Could Address Fetal Alcohol Syndrome

AUGUSTA, Ga. Providing dietary substrates such as betaine or citicoline to support biosynthesis of sphingomyelin (SM) from ceramide may prevent ethanol-induced damage of certain neural cells associated with fetal alcohol syndrome (FAS), according to a new study (Cell Death Dis. ePub 27 May 2010; DOI: 10.1038-cddis.2010.22). Researchers from the Medical College of Georgia, Augusta, first used neural crest-derived cell (NCC) cultures from mouse embryos to determine why certain embryonic tissues are sensitive toward ethanol. Apoptotic cells stain intensely for ceramide, suggesting ceramide-induced apoptosis mediates ethanol damage to NCCs. Adding CDP-choline (citicoline) to the cultures reduced apoptosis; citicoline is a precursor for the conversion of ceramide to SM.

The research team then intubated pregnant mice with ethanol, resulting in ceramide elevation and increased apoptosis of NCCs. The exposure was concurrent with malformation of parietal bones in 20 percent of embryos. Production of meninges, a tissue complex derived from NCCs, was also disrupted, generating reduced levels of TGF-beta-1, a growth factor critical to bone and brain development. According to the researchers, this disruption could explain the development of cranial bone malfunction and cognitive dysfunction in FAS. They suggest treatment with citicoline could alleviate the tissue damages induced by ethanol.