Home Overview Press Room Blog Publications For Students about us

Fresh concerns raised over controversial 'three parent baby' therapy which aims to eliminate inherited disease

The Irish Examiner
July 6th, 2016

A brown mouse in the hand of a scientist wearing a blue glove.

Hidden effects on metabolism and ageing may make it harder to rid future generations of devastating inherited diseases using a controversial “three parent baby” treatment, new research suggests.

Scientists working with mice found that an early mismatch of DNA had disturbing consequences later in life, including accelerated ageing.

Whether humans might respond the same way is not yet known. But the research raises new concerns about attempts to eliminate inherited disease by replacing defective mitochondrial DNA.

Last year Parliament took the bold step of approving mitochondrial replacement therapy, which would allow DNA in human embryos to be altered in a way that affects future generations.

Mitochondrial DNA (mtDNA) is separate from the genetic material in the cell nucleus that determines physical characteristics such as facial features, eye colour, and most of the body’s biology.

Housed in rod-like bodies in the cell called mitochondria, it accounts for 0.1% of human DNA, but has important metabolic functions linked to the conversion of food to energy.

Inherited flaws in mtDNA, which is only passed from mothers to their children, result in mitochondrial diseases which can have terrible effects, including muscle wasting, blindness and dementia.

The “three parent” solution involves replacing a human embryo’s faulty mtDNA with a healthy version from a female donor – the “third” parent.

Last month UK scientists led by a team from the University of Newcastle announced the results of tests on more than 500 donated eggs that appeared to show the technique would lead to normal pregnancies.

The work paves the way for the first attempt to conceive an IVF baby from the cells of three people to prevent mitochondrial disease.

Findings from the new study, published in the journal Nature, indicate that nuclear and mitochondrial DNA interact – and when they are not matched, harmful effects can result.

The Spanish researchers studied specially bred strains of mice which had the same nuclear DNA but different mtDNA.

When the animals were young they seemed to be in good health, but as they aged problems arose affecting metabolism, obesity, and lifespan.

One key finding was shortening of telomeres – protective caps on the ends of chromosomes – which signifies accelerated ageing.

Lead scientist Dr Jose Antonio Enriquez, from the CNIC (Centro Nacional de Investigaciones Cardiovasculares Carlos III) research institute in Madrid, said the results highlighted the importance of avoiding a mismatch between mtDNA and nuclear DNA.

He said: “Just as with organ transplantation and blood transfusion, it is important to select mitochondrial donors, to ensure that the new mitochondrial DNA is genetically similar to that of the mother whose eggs require mitochondrial DNA replacement.”

Having to find suitable mtDNA donors with a good enough genetic match would greatly complicate the business of applying the technology to free families of the curse of mitochondrial disease.

Research has shown that mitochondrial donation could potentially help almost 2,500 women of reproductive age in the UK who are at risk of transmitting the conditions to their babies.

Critics including church leaders and pro-life groups, have warned that the change has been brought about too hastily and marks the start of a “slippery slope” towards designer babies and eugenics.

Dr Dusko Ilic, reader in stem cell science at King’s College London, said the concept of interaction between mitochondrial and nuclear DNA was “fascinating and mind-boggling”.

He said: “Should this study influence our thinking when considering mitochondrial replacement for prospective mothers harbouring pathogenic mtDNA mutations? Clearly, the safest and most simple option is to ensure the donor mtDNA genotype is as similar to the recipient genotype as possible.”

He added: “Obviously the study has to be repeated on animals that are not inbred, and species other than mice, before we can extrapolate the phenomenon to humans.

“At that stage we can worry whether a pre-selection of mitochondrial donor should be considered for the emerging field of preventing transmission of mitochondrial DNA disease by mitochondrial replacement therapy in human eggs.”

Professor Robert Lightowlers, director of the Institute for Cell and Molecular Biosciences at the University of Newcastle, called the study “remarkable”.

Image via Wikimedia

This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of biotechnology and public policy issues. We believe this constitutes a 'fair use' of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes. For more information go to: http://www.copyright.gov/title17/92chap1.html#107. If you wish to use copyrighted material from this site for purposes of your own that go beyond 'fair use', you must obtain permission from the copyright owner.


home | overview | blog | publications| about us | donate | newsletter | press room | privacy policy

CGS • 1122 University Ave, Suite 100, Berkeley, CA 94702 • • (p) 1.510.665.7760 • (F) 1.510.665.8760