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. 2019 Jan 28;7:2050312118823585. doi: 10.1177/2050312118823585

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© The Author(s) 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 6. — A hypothetical mechanism involving dysfunctions of hedonic feeding and the development of hyperphagia phenotypes in AS and PWS. PWS and AS may involve opposite dysfunctions of dopaminergic pathways due to losses and gains in dosages of imprinted genes. The effect is more pronounced with uniparental disomies and imprinting defects due to an increased dosage of paternally (or maternally) expressed genes. The increased dosage of paternally expressed genes and the expected increases in dopamine levels may explain the tendency for selective eating and the early development of hyperphagia in AS associated with patUPD and imprinting defects.