'Three-parent baby' success could see trials in two years

Stephanie Uhlenbrock/Plainpicture By Andy Coghlan   A controversial “three-parent” gene fertility treatment has been tested successfully in healthy human embryos for the first time. The treatment aims to create embryos free of hereditary mitochondrial disease, and may now be considered safe enough to start human trials within one to two years. The potential beneficiaries would be children otherwise at risk of serious disease because their mothers pass down defective mitochondria, the “power packs” that provide energy to all living cells. Without healthy mitochondria, children can develop a range of degenerative disorders because their cells don’t work properly. The faulty mitochondria reside in the body of the egg, separated from the rest of its DNA, which is stored in the nucleus. Researchers have developed a technique that prevents this mitochondria from being passed on by fertilising the egg, then removing the nucleus and transferring it into a nucleus-free egg from a donor with healthy mitochondria. The resulting embryo has DNA from the father and mother, as well as a tiny amount of mitochondrial DNA from the donor. In 2010, Doug Turnbull of the Wellcome Trust Centre for Mitochondrial Disease at Newcastle University, UK, and his colleagues showed that the technique worked, but at the time its safety could not be verified. That’s because they used donor eggs discarded from IVF treatments because of defects, so it was not possible to find out if healthy embryos could result. Now they have performed the same technique more than 200 times using healthy donor eggs. “We can’t say any procedure is 100-per-cent safe,” says Turnbull. “I think we have to move along respectfully and appropriately, but as a group of scientists and clinicians, we are working as hard as possible to make this available to patients.” In earlier experiments, Turnbull’s team found that some of the faulty mitochondrial DNA still ended up in the embryo, because residues of fluid from the mother’s egg stick to the nucleus when it is extracted. Now, the technique has been improved to reduce the amount of faulty mitochondria carried over. This was achieved through more careful extraction of the nucleus, and from manipulating the chemical solution used during extraction. Of the embryos created, 79 per cent had less than 2 per cent faulty mitochondrial DNA. And in 42 per cent of those there was no detectable faulty mitochondrial DNA at all. Putting this in perspective, the amount of defective mitochondrial DNA you would expect to see in a natural conception by a woman carrying the disease would vary from under 10 to 100 per cent of mitochondrial DNA. Generally, children remain free of the disease provided the amount of defective mitochondrial DNA is below 30 per cent. The team also increased the survival rate of embryos by extracting the nucleus sooner after fertilisation – within 8 hours instead of 24. “We think it gives the embryos longer to recover from being extracted before they divide to the two-cell stage,” says Mary Herbert, co-leader of the Newcastle team. Early extraction raised the survival rate from 40 to 90 per cent. Although the resulting embryos were almost indistinguishable in terms of quality and function of genes from those created through normal IVF, there was one setback. The team discovered that in some of the cells extracted from the “three-parent embryos”, levels of defective mitochondrial DNA increased as the cells multiplied. “It sounds a note of caution for us,” says Turnbull. The UK Human Fertilisation and Embryology Authority is expected to examine all the evidence later this year, after which time they will make a decision whether to issue the Newcastle team with a licence to treat the first patient. Journal reference: Nature, 10.1038/nature18303 More on these topics:
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