to result from the peroxidation of 7DHC and its derivatives, inhibiting this peroxidation would likely have beneficial effects. Antioxidants have been shown to increase the level of lipid transcripts in SLOS cells, these transcripts play a role in lipid (cholesterol) biosynthesis and are known to be down-regulated in SLOS. Furthermore, vitamin E specifically is known to decrease DHCEO levels, which is an indicator of oxidative stress in SLOS, as well as present beneficial changes in gene expression. Vitamin E appears to be the most powerful antioxidant for treating SLOS, and in mouse models has reduced the levels of oxysterols in the brain. However, antioxidants have only been studied in animal models of SLOS or isolated SLOS cells. Thus, their clinical significance and negative side effects are still unknown, and their use has yet to be studied in humans. Further considerations When treating SLOS, a recurring issue is whether or not the intellectual and behavioural deficits are due to fixed developmental problems (i.e. fixed brain malformations), or due to ongoing abnormal sterol levels that interrupt the normal function of the brain and other tissues. If the latter is true, then treatments which change the sterol levels and ratios, particularly in the brain, will likely improve the developmental outcome of the patient. However, if the former is true, then treatment is likely to help only with symptoms and not with specific developmental deficits. Research The most common animal used to study SLOS is the mouse. According to BioCyc, cholesterol biosynthesis in mice is very similar to that of humans. Most importantly, mice possess both DHCR7 (the enzyme responsible for SLOS), and HMG-CoA reductase (the rate limiting step of cholesterol synthesis. Rats are similar to mice and have also been used. There are two popular ways in which animal models of SLOS are created. The first is using teratogens, the second is using genetic manipulations to create mutations in the DHCR7 gene. Teratogenic models Teratogenic models are induced by feeding pregnant rats or mice inhibitors of DCHR7. Two common inhibitors are BM15766 and AY9944 . These compounds have different chemical and physical properties, but induce similar effects. AY9944 has been shown to induce holoprosencephaly and sexual malformations similar to those seen in humans with SLOS. It is also known to cause impairments in the serotonin receptor, another defect commonly seen in SLOS patients. BM15766 has produced the lack of cholesterol and bile acid