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Alan E.H. Emery

, Francesco Muntoni

, and Rosaline C.M Quinlivan

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date: 16 July 2020

When this book was first written, much space was given to evidence of vascular, neurogenic, and membrane hypotheses of causation. With the discovery that the primary cause was deficiency of dystrophin located at the cell membrane, there seemed no longer reason to consider previous research. However, there may be important ideas necessary for a full understanding of the disease process. Thus, although a vascular or neurogenic defect is not the primary cause, the contribution of an inaequate blood supply to muscle might aggravate the disease process. Proper functioning and organization of the neuromuscular junction are essential for the correct differentiation of muscle fibres. We do not know if such influences, in addition to a deficiency of muscle dystrophin during muscle development, might contribute to the full expression of an abnormal phenotype. With recent advances in understanding of the cellular partners of dystrophin, a complex pathogenic scenario of functions has emerged.

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