Whereas it previously has been demonstrated that CR significantly reduces amyloid deposition in Tg AD model mice, it is likely that the limited change in Ab levels in our CR animals is related to the relatively low level of CR used in this study compared to the higher levels of CR used in most studies. The ELISA data show, however, that there is a reduction in the amounts of insoluble Ab in both LY and CR groups. Plaques in this AD mouse model are typically accompanied by activated glial cells, both astrocytes and microglia. The role of the activated glial cells is unclear. On the one hand, they may protect the brain by removing Ab. On the other hand, they secrete inflammatory cytokines and generate nitric oxide and can thus damage and kill bystander neurons. The role of activated microglia cells in the uptake of Ab is disputed, with some evidence suggesting Ab is cleared by microglia, whereas other evidence suggests that microglia do not clear Ab. Plaques in the control animals in our experiment were surrounded by activated glial cells; however, in both the LY and CR mice, the dense amyloid b deposits were associated with much lower activated microglia. This suggests that both CR and ghrelin in the absence of hunger reduce the inflammatory response to deposited Ab, thus evoking a smaller inflammatory response from microglial cells, similar to what has been reported in other studies. At the end of the study, the CR animals did not show a significant increase in body weight, while both LY and control animals had a similar increase in body weight. Similarly, the QMR fat mass data show that the CR mice had significantly lower fat mass compared to the other two groups. Weight loss is a characteristic finding of patients with Alzheimer??s disease. It seems that it precedes cognitive impairment by some years, but the underlying causes are not fully understood. Both ghrelin and leptin are involved in energy homeostasis and may be the effect astrocytes had on dopaminergic neurons is unclear antagonist treated animals.In the present study, we determined the tissue-specific imprinting status of IGF2R in first trimester Bos taurus concepti generated in-vivo or in-vitro. We quantified variation in allele-specific expression bias, i.e. expression of the repressed paternal allele relative to the predominantly expressed maternal allele, determined methylation levels in DMR2, and analyzed relationships between expression bias and fetal phenotype in fetuses with or without overgrowth after in-vitro fertilization procedures with embryo culture. Our data show that in all fetal tissues but brain, Bos taurus IGF2R is imprinted and predominantly expressed from the maternal allele as in mouse. However, in contrast to mouse, we detected partial imprinting in placenta that could be related to differences in reproductive strategy between cow and mouse. Contrary to expectations, imprinting and DNA methylation were not affected by IVF with in-vitro embryo culture and there was no correlation between minor variation in inter-individual allele-specific expression bias and fetal weight.