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

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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 childhood, syndromes presenting with mental retardation and obesity should be taken into account (Bardet-Biedl syndrome, Cohen syndrome and Albright hereditary osteodystrophy) [19]. Angelman Syndrome The disorder, first described in 1965 by Angelman, has an estimated incidence between 1 in 10,000 and 1 in 40,000.

More recently, Abmayr et al. [31] demonstrated that co-injection of the rAAVmicrodystrophin and rAAV-mIGF-1 vectors resulted in increased muscle mass and strength, reduced myofiber degeneration, and increased protection against contraction-induced injury. These results suggest that a dual-gene, combinatorial strategy could enhance the efficacy of gene therapy of DMD and underscored the importance of rAAV vectors due to their relative lack of immunologic and toxic side effect combined with their potential for body-wide systemic gene delivery to muscle [31].

It has been also reported that, unlike mature IGF-1, the distinct E domain of MGF inhibits terminal differentiation whilst increasing myoblast proliferation [15]. The determination of E peptide function and fate awaits the availability of epitope-specific antibodies, since it is unclear when or whether E peptides are cleaved from the mature IGF-1 protein. Notably, E peptide IGF-1 Counteracts Muscle Wasting 31 splicing patterns are different in the human gene [16], an anomaly that will need to be considered in the future when translating the results of animal research into clinical applications.

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