Preventing the transmission of pathogenic mitochondrial DNA mutations: Can we achieve long-term benefits from germ-line gene transfer?

Should this be a cause for concern, and how low must the maternal mtDNA carry-over be in order to consider these therapies successful? These questions will be difficult to address experimentally because current animal models of mtDNA disease do not closely resemble human disorders ( Nakada and Hayashi , 2011 ) and there may be significant differences in the mechanism of mtDNA transmission (i.e. the mtDNA bottleneck) between humans and mice ( Wonnapinij et al ., 2010 ).

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