Apolipoprotein E deficiency alters the uptake of radioactive vitamin E by different regions of the brain

We have observed that apoE deficiency reduces brain levels of vitamin E (Vatassery et al. J. Neurosci. Res . 84 : –72, 2006). As an extension of these studies we examined the uptake of labeled alpha tocopherol by brains from 11 weeks‐old apoE deficient mice fed normal rodent chow. Intravenously injected, tritium‐labeled alpha tocopherol was poorly transported to the brain. Hence labeled alpha tocopherol was injected into the lateral cerebral ventricle. Labeled cholesterol was injected simultaneously and the data was used as an internal standard to account for experimental variability of injections etc. As expected, regions close to the site of injection and those with high surface areas in contact with spinal fluid showed higher uptake of radioactive alpha tocopherol (e.g., hippocampus and striatum more than cerebral cortex). Most areas of apoE deficient brains showed a decrease in uptake of radioactive tocopherol per gram wet weight. Alterations in the clearance and transport of tocopherol (possibly mediated by apoE) might be the reason for this decline in uptake. Nearly all of the injected alpha tocopherol was unchanged in the brains of both apoE deficient and wild type animals suggesting low turnover rate. Overall, the current data reinforce the hypothesis that apoE is a key protein involved with the transport and/or retention of alpha tocopherol in brain. Supported by Dept. of Veterans Affairs, Washington DC.