Abstract
The cogenital muscular dystrophies (CMDs) have seen enormous progress as regards the recognition of nosologic entities, the elucidation of pathophysiology, and therapeutic approaches based on this understanding. This review will focus on the disorders which are not caused by abnormalities of α-dystroglycan. For laminin α2 deficiency the results with the most promising therapeutic potential have been obtained by gene engineering strategies reinforcing the basement membrane-dystroglycan link by agrin or perlecan constructs, or substituting laminin α2 by other laminin chains.
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