71 genes in 22 chromosomal regions in mice (29 of the same genes are imprinted in both humans and mice)130. The authors speculated that the total numbers of imprinted genes are probably not much greater than these estimates, although they acknowledged the possibility that additional imprinted genes with more subtle phenotypic effects probably exist. They cite in support of the latter the large number of complex diseases with parent-of-origin effects, including asthma, autism, type I and type II diabetes, Alzheimer disease, and schizophrenia. For these diseases, the risk for disease in the child differs depending on whether the mother or father is likewise affected, or whether a particular risk allele is inherited from the mother or from the father. Some of these effects may reflect as yet unidentified imprinted loci. In fact, a recent genome-wide analysis of genomic imprinting in mice revealed evidence for parent-of-origin effects due to genomic imprinting on a wide range of quantitative phenotypes related to body size and growth rates, and for imprinting effects that varied over time and which arose or persisted into adulthood133. Therefore, some of the sex-specific parent-of-origin effects observed in complex human diseases, such as those mentioned above, may be attributable to
