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By Marco Cappa, Mohamad Maghnie, Sandro Loche, Gian Franco Bottazzo

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Extra resources for Endocrine Involvement in Developmental Syndromes (Endocrine Development Vol 14)

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Mental retardation is in the mildto-moderate range and most patients have an IQ ranging from 60 to 70. Many show an unusual skill in doing jigsaw puzzles, suggesting a particular attention to visual details. Behavioral problems are frequent and include not only food-related problems (excessive appetite, absent sense of satisfaction, obsession with eating), but also temper tantrums, impulsivity, sleep disturbance, skin picking, obsessive-compulsive symptoms and anxiety [14, 17]. The genetic abnormality of PWS is the lack of expression of paternally inherited genes in chromosome 15q11-q13.

Approximately 70% of affected individuals have a cytogenetically small deletion of chromosome segment 15q11-q13. Maternal uniparental disomy (UPD) accounts for 25%, imprinting defect (small deletion or mutation) for 2–5% and the remaining <1% is due to chromosomal rearrangement involving proximal 15q (fig. 3). Patients with UPD or imprinting defect generally have a milder phenotype than those with deletions [14]. The differential diagnosis for PWS in infancy includes many causes of neonatal hypotonia, Prader-Willi and Angelman Syndromes 25 particularly neuromuscular disorders.

In mammalian embryos there are two major cycles of epigenetic reprogramming of the genome: during preimplantation and during germ cell differentiation. These events have been widely studied in mouse embryos. After fertilization, the paternal and maternal genomes undergo a genomewide demethylation, followed by de novo methylation around the time of implantation. Imprinted alleles are protected from this wave of demethylation and Prader-Willi and Angelman Syndromes 21 remethylation to maintain their proper dosage effects.

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