Born of science: Spindler, a baby rhesus macaque, is one of only four monkeys born with DNA from three parents.
Credit: Nature

A new method tested in monkeys for replacing mitochondrial DNA could one day prevent devastating diseases.

MIT Technology Review, September 1, 2009, by Lauren Gravitz  —  Mitochondrial diseases, which affect as many as one in 4,000 people, can impair muscles, nerves, even entire organ systems, and have no known cure. Now, in a breakthrough study, Oregon researchers replaced defective mitochondrial DNA with that from a healthy donor. The first subjects, four baby monkeys, are pushing the envelope on the ethical debate that surrounds bioengineering.

Mitochondria are often called the cell’s power plants–the tiny organelles are responsible for energy production, and there can be hundreds to thousands of them in a single cell. They also contain their own DNA. Unlike nuclear DNA, which is a unique combination of both parents’ genomes, mitochondrial DNA (or mtDNA) is passed down through the mother, is derived almost exclusively from her egg, and typically remains unchanged from one generation to the next. Mutations in a woman’s mtDNA are inherited by her child, and so far there has been no way to cure these conditions or stop their transmission.

Now, Shoukhrat Mitalipov and his colleagues at Oregon Health & Science University in Beaverton, OR, have found a way to get rid of mutant mtDNA. Using a process similar to cloning, they first harvested a fertile egg. Then, when the egg was undergoing cell division, they removed a set of its chromosomes and inserted them into an egg harvested from another female, one that already had its nucleus removed. In essence, the enucleated egg provided a set of mitochondrial chromosomes, while the transferred nuclear chromosomes provided the main genetic material for development. Other researchers have attempted similar processes, but previous efforts couldn’t prevent mutant mitochondria from tagging along to the new egg.

The researchers avoided this problem by carefully isolating chromosomes during a very specific and segregated process of cell division, in which nuclear DNA is tied up into an elliptical spindle. “Our whole technique comes to efficiently separating the two different types of DNA that [mammals] carry, and to separate them very cleanly,” Mitalipov says. “We believe this can be used to prevent transmission of mutated mitochondrial DNA…[and] correct for mitochondrial DNA mutations in children even before they’re born.”

To date, there are 200 to 250 known disease-causing mutations in mitochondrial DNA, and they occur in as many as one in 4,000 people. The syndromes vary in severity, with symptoms ranging from muscle weakness and loss of motor control to diabetes, liver disease, and developmental delays. Many die before ever reaching adulthood. “The patients carrying these types of mutations don’t have the same options for genetic counseling,” Mitalipov says, since any mutation a woman has will be passed to her egg. “Currently, her only options are using donated eggs or adopting a child.”

“It’s an important study, and it’s the only approach that I can think by which you could render a family free of risk of their offspring developing a mitochondrial DNA disease,” says Douglas Wallace, a mitochondrial DNA researcher at the University of California, Irvine. Because mitochondrial DNA is self-replicating, the technique allows for a way to “swap” healthy versions for mutant ones without genetic alterations.

But therein also lies the rub. Many researchers and ethicists alike balk at the idea of making genetic changes to the germline, ones that fundamentally affect an egg or sperm and will be passed along to the next generation. While swapping out mitochondrial DNA may not qualify as the kind of germline engineering people have in mind when they worry about made-to-order babies–with certain traits like intelligence or eye color specifically engineered–it edges toward that shaky ethical ground.
“The technique that they used, transferring a chromosomal spindle to get new mitochondria to power the egg, seems completely ethical and defensible,” says Arthur Caplan, a bioethicist at the University of Pennsylvania. “But while this technique doesn’t have much use outside of fixing problems in the mitochondria, it does open the door a tiny bit on germline engineering.” Because it’s using a self-contained part of the cell, he notes that it’s not what people typically have in mind when they talk about tinkering with germline genetics. “But by cracking open the door, it puts the principle of never doing germline engineering into dispute.”

David Magnus, who heads Stanford University’s Center for Biomedical Ethics, agrees that most of society’s germline engineering concerns don’t apply in this case. But he does point out that the procedure would lead to, essentially, three parents instead of two, “making legal and social arrangements more complicated,” he says. “What happens if the mitochondrial donor decides, down the road, that she should have some parental rights to the offspring?”

This is, of course, getting way ahead of the science itself. Much more must be done before the procedure is approved. The new technique has only been applied in nine rhesus macaques, three of which became pregnant (one with twins)–a 33 percent success rate that appears to mirror that of regular in vitro fertilization in human patients. And since the seemingly healthy offspring have not yet reached reproductive age, Mitalipov and his colleagues don’t yet know whether the procedure has genetic implications they’ve not yet uncovered. The procedure will also need to be refined, tested in more than nonhuman primates and at other research facilities before human trials can begin. (The Oregon lab is known for very high success rates that other labs can rarely duplicate.)

Researchers in Britain, at the University of Newcastle upon Tyne, have reportedly done something similar in human embryos, but have yet to publish their results and would not comment on Mitalipov’s research.

The Oregon researchers believe they may be ready to apply for clinical trials in two to three years, but much depends on funding and government approval. “This points the way to a technique–it doesn’t provide a therapy,” says UC Irvine’s Wallace, who was the first researcher to discover disease-causing mutations in mitochondrial DNA. “It shows that the concept can work as one approach to treating mitochondrial DNA disease. And that’s an incredible advance, since we have very little to offer these families right now.”


Can regenerative medicine defeat ageing?
By Aubrey D.N.J. de Grey
Chief Science Officer, SENS Foundation

Appeared in BioNews 520

Ieet.org, August 31, 2009  —  The relevance of nearly all biogerontology research to combating aging is restricted to the potential for slowing down the accumulation of molecular and cellular damage that eventually leads to age-related ill-health. Meanwhile, regenerative medicine has been progressing rapidly and is nearing clinical applicability to a wide range of specific conditions. My view is that we are approaching the point where regenerative medicine can be used against aging. This would entail not retarding but actually reversing the accumulation of damage. If successful, this would obviously be a far more valuable technology than mere slowing of aging. However, in order to be successful it must be comprehensive, and some aspects of aging may seem impossible to address in this way. In fact, however, it seems that all types of molecular and cellular damage which contribute to age-related ill-health are realistic targets of regenerative interventions.

The human body is, ultimately, a machine – an astronomically complex machine, of whose workings we remain pitifully ignorant – but still a machine. Like any machine, it accumulates ‘damage’ as a side-effect of its normal operation: molecular and cellular changes that occur throughout life are initially harmless, but eventually (when too abundant) increasingly impede the normal operation of the machine and eventually cause it to fail altogether. Conceptually, there are three strategies to postpone a machine’s demise beyond its ‘warranty period’. First, we can treat it really well throughout its life, thereby slowing down the accumulation of damage: but that can never stop the accumulation altogether, because to do so would require not operating the machine at all, and anyway it cannot address damage that has already occurred. Alternatively, we can combat the late-life symptoms, the dysfunction that eventually emerges: but that too is only a short-term approach, because the underlying damage that causes the dysfunction is still accumulating and making the dysfunction harder and harder to address. This is why the way in which machines that people love are in fact kept in good shape is the third strategy: repair and maintenance, in which we let the damage be created, but repair it before it becomes so severe as to cause dysfunction. In the case of the human body, this means using regenerative medicine against aging.

So… can it work? Are all the types of damage that contributed to age-related ill-health amenable to repair?

If ‘repair’ is interpreted strictly, there are two classes of damage for which the answer to this question is probably ‘No’. They are mutations in the nuclear and mitochondrial DNA. However, a better way to interpret the term ‘repair’ is ‘repair for practical purposes’ – and here the scene is rosier. Mitochondrial mutations may not be feasible to remove, but it may be much more feasible to eliminate their consequence, dysfunctional mitochondria, by complementing their mutations with nuclear transgenes – a goal that has long seemed quixotic but has now largely been achieved by Corral-Debrinski’s group. In the case of nuclear mutations (and epimutations, i.e. disruptions of the decorations to DNA that determine its expression pattern), a different end-run seems available: to focus on the consequences of those mutations at the level of cell number, which come down to inadequate cell death or excessive cell division. Both these classes of problem are potentially amenable to reversal – by suicide gene therapy and by telomere maintenance abrogation, respectively. (Mutations that deplete cell number do not accumulate, by definition: the loss of cells is a part of aging, but it can potentially be addressed by stem cell therapies.)

What about nuclear mutations/epimutations that do not affect cell number? My interpretation of the available data is that such damage simply does not accumulate fast enough to matter in anything like a currently normal lifetime: the imperative to avoid cancer until procreation has driven evolution to develop DNA repair and maintenance machinery that is ‘unnecessarily good’ in respect of other mutations.

Other types of damage exist that are probably also too slow to matter. Some are for the same ‘protagonistic pleiotropy’ reason: glycation-induced adducts such as carboxymethyl-lysine, for example, are limited in abundance because they arise by the same process that also causes protein-protein crosslinks (particularly glucosepane), whose effects are much more potent. (Crosslinks themselves need to be addressed, and much work is in progress to develop ways to cleave them.) Aspartate racemisation of long-lived proteins also accumulates, but its effects seem to be minimal.

In conclusion, regenerative medicine – if appropriately broadly defined – seems to have a fighting chance of combating aging within the next decade in laboratory mammals and within perhaps 25-30 years in humans. Since its health benefits would so immensely exceed those of the best possible ‘gerontology’ and ‘geriatrics’ approaches, there is a clear case for rapidly prioritizing efforts to develop such interventions.

Aubrey de Grey is organizing the 4th conference on Strategies for Engineered Negligible Senescence in Cambridge on 3-7 September 2009. 


Aubrey David Nicholas Jasper de Grey (born 20 April 1963 in London, England) is an English author and theoretician in the field of gerontology.


De Grey is the author of the mitochondrial free-radical theory of aging, and the general-audience book Ending Aging, a detailed description of how regenerative medicine may be able to thwart the aging process altogether within a few decades. He works on the development of what he has termed “Strategies for Engineered Negligible Senescence” (SENS) – a tissue-repair strategy intended to rejuvenate the human body and thereby allow an indefinite lifespan. To this end, he has identified seven types of molecular and cellular “damage” caused by essential metabolic processes; SENS is a proposed panel of therapies to repair this damage.The scientific community is skeptical of de Grey’s claims; a review of SENS by 28 scientists concluded that none of de Grey’s therapies “has ever been shown to extend the lifespan of any organism, let alone humans”.

De Grey has been interviewed in recent years in many news sources, including CBS 60 Minutes, BBC, the New York Times, Fortune Magazine, the Washington Post, TED, Popular Science and The Colbert Report. His main activities at present are as Chief Science Officer of the SENS Foundation and editor-in-chief of the academic journal Rejuvenation Research.


Aubrey de Grey was educated at Sussex House School and Harrow School. In 1985 he received a B.A. in Computer Science from Trinity Hall, University of Cambridge and joined Sinclair Research Ltd as an AI/software engineer; in 1986, he co-founded Man-Made Minions Ltd to pursue the development of an automated formal program verifier. Until 2006, he was in charge of software development at the University of Cambridge Genetics Department for the FlyBase genetic database.

In 2000 Cambridge awarded de Grey a Ph.D. on the basis of his book concerning the biology of one aspect of aging, The Mitochondrial Free Radical Theory of Aging (ISBN 1-58706-155-4), which he wrote in 1999. The book controversially claimed that obviating damage to mitochondrial DNA might by itself extend lifespan significantly, though it stated that it was more likely that cumulative damage to mitochondria is a significant cause of senescence, but not the single dominant cause. A February 8, 2007 search for “de Grey AD [au]” on PubMed revealed 61 publications in 25 peer-reviewed journals, of which 19 are in Rejuvenation Research (impact factor 4.728), the journal edited by de Grey.

Regarding his background as a computer scientist (and subsequently a bioinformatician in genetics), de Grey states:

“There are really very important differences between the type of creativity involved in being a scientist and being a technical engineer. It means that I’m able to think in very different ways and come up with approaches to things that are different from the way a basic scientist might think.”


De Grey argues that the fundamental knowledge needed to develop effective anti-aging medicine mostly already exists, and that the science is ahead of the funding. He works to identify and promote specific technological approaches to the reversal of various aspects of aging, or as de Grey puts it, “the set of accumulated side effects from metabolism that eventually kills us, and for the more proactive and urgent approaches to extending the healthy human lifespan. Regarding this issue, de Grey is a supporter of life extension.

As of 2005, his work centered upon a detailed plan called Strategies for Engineered Negligible Senescence (SENS), which is aimed at preventing age-related physical and cognitive decline. In March 2009, Aubrey de Grey co-founded the SENS Foundation, a non-profit organization based in California, United States, where he currently serves as Chief Science Officer. The Foundation “works to develop, promote and ensure widespread access to regenerative medicine solutions to the disabilities and diseases of aging,” focusing on the Strategies for Engineered Negligible Senescence. De Grey is also co-founder (with David Gobel) and former Chief Scientist of the Methuselah Foundation, a 501(c)(3) nonprofit organization based in Springfield, Virginia, United States. A major activity of the Methuselah Foundation is the Methuselah Mouse Prize, a prize designed to hasten the research into effective life extension interventions by awarding monetary prizes to researchers who stretch the lifespan of mice to unprecedented lengths. Regarding this, de Grey stated in March 2005 “if we are to bring about real regenerative therapies that will benefit not just future generations, but those of us who are alive today, we must encourage scientists to work on the problem of aging.” The prize reached 4.2 USD million in February 2007. De Grey believes that once dramatic life extension of already middle-aged mice has been achieved, a large amount of funding will be diverted to this kind of research, which would accelerate progress in doing the same for humans.

De Grey has published papers in this area in prominent journals with some of biogerontology’s foremost researchers, including Bruce Ames, Leonid Gavrilov and S. Jay Olshansky, as well as other thinkers such as Gregory Stock. He has also received support from other prominent scientists, such as William Haseltine, the biotech pioneer of Human Genome Sciences, who in March 2005 stated regarding the Methuselah Mouse Prize “there’s nothing to compare with this effort, and it has already contributed significantly to the awareness that regenerative medicine is a near term reality, not an if.”

In 2005, he was the subject of a critical article in MIT‘s Technology Review.  See de Grey Technology Review controversy.

In 2007, de Grey wrote the book “Ending Aging” with the assistance of Michael Rae.  It summarizes the science, politics and social challenges of the entire SENS agenda.

In a 2008 broadcast on the Arte German & French TV, de Grey confirmed that according to him, the first man who will live up to 1,000 years is probably already alive now, and might even be today between 50 and 60 years old.

The seven types of aging damage proposed by de Grey

Main article: Strategies for Engineered Negligible Senescence

  1. Cancer-causing nuclear mutations/epimutations:

These are changes to the nuclear DNA (nDNA), the molecule that contains our genetic information, or to proteins which bind to the nDNA. Certain mutations can lead to cancer, and, according to de Grey, non-cancerous mutations and epimutations do not contribute to aging within a normal lifespan, so cancer is the only endpoint of these types of damage that must be addressed.

  1. Mitochondrial mutations:

Mitochondria are components in our cells that are important for energy production. They contain their own genetic material, and mutations to their DNA can affect a cell’s ability to function properly. Indirectly, these mutations may accelerate many aspects of aging.

  1. Intracellular aggregates:

Our cells are constantly breaking down proteins and other molecules that are no longer useful or which can be harmful. Those molecules which can’t be digested simply accumulate as junk inside our cells. Atherosclerosis, macular degeneration and all kinds of neurodegenerative diseases (such as Alzheimer’s disease) are associated with this problem.

  1. Extracellular aggregates:

Harmful junk protein can also accumulate outside of our cells. The amyloid plaque seen in the brains of Alzheimer’s patients is one example.

  1. Cell loss:

Some of the cells in our bodies cannot be replaced, or can only be replaced very slowly – more slowly than they die. This decrease in cell number causes the heart to become weaker with age, and it also causes Parkinson’s disease and impairs the immune system.

  1. Cell senescence:

This is a phenomenon where the cells are no longer able to divide, but also do not die and let others divide. They may also do other things that they’re not supposed to, like secreting proteins that could be harmful. Immune senescence and type 2 diabetes are caused by this.

  1. Extracellular crosslinks:

Cells are held together by special linking proteins. When too many cross-links form between cells in a tissue, the tissue can lose its elasticity and cause problems including arteriosclerosis and presbyopia.

Technology Review debate

Main article: De Grey Technology Review debate

A debate over the validity of the de Grey’s theories on ageing was published in MIT‘s Technology Review. In the end, none of the challengers to de Grey were able to convince the judges that SENS was “so wrong that it is unworthy of learned debate.”

Scientific journal

Titles and positions

De Grey is a fellow of the Institute for Ethics and Emerging Technologies and an advisor for the Singularity Institute.

Can We Avoid Aging?

An American Couple Tried It For 30 Days……………..take a look.


By Tina McCarthy, EcoSalon. Posted September 1, 2009. 

Incorporate these healthy foods into your diet to strengthen your immune system in a way your taste buds can appreciate.

Not in the mood to choke down yet another gritty serving of Emergen-C? Boost your body from the inside out with powerful foods that help your immune system function optimally. Just incorporate these healthy foods into your diet to strengthen your immune system in a way your taste buds can appreciate.

  • Oysters


Packed with selenium, this tasty shellfish helps boost your body’s production of cytokines, a protein that’s known to ward off illnesses.

  • Yogurt


Yogurt that contains live cultures is rich in lactobacillus acidophilus and bifidobacterium lactis (read: good bacteria), which fight bacteria that cause diseases and raise your white blood cell count. 

  • Green Tea


Green tea is a great source of L-theanine, an amino acid that triggers the release of germ-fighting compounds from your T-cells. (Green tea also helps to boost your metabolism.) 

  • Oranges


One of the best sources of immunity-boosting vitamin C, oranges cause your body to produce higher levels of antibodies and white blood cells.

  • Crab


Like oysters, crab meat is rich in selenium, a nutrient that strengthens your immune system. 

  • Garlic


Garlic is loaded with ajoene, allicin and thiosulfinates, compounds high in sulfur that ward off diseases and help battle infections. 

  • Carrots


Carrots are crammed with beta carotene, a phytonutrient that increases your body’s production of T-cells and natural killer cells.

  • Spinach


The high amount of antioxidants found in spinach help boost your immune system. 

  • Sweet Potatoes


Like carrots, sweet potatoes are loaded with beta carotene, which boosts your body’s T-cell and NK-cell count. 

  • Mushrooms


Rich in compounds called beta glucans, mushrooms boost the production of NK-cells and T-cells in your body to help prevent infections. 

  • Salmon


Salmon contains omega-3 fatty acids, which cause your body’s phagocytes to fight bacteria more effectively. 

  • Kiwi


Like oranges, kiwis are high in vitamin C, which helps protect your body against infections. 

  • Bell Peppers


Bell peppers are packed with vitamin C, which prompts your body to produce more interferon. This antibody covers the surface of cells and fends off viruses. 

  • Broccoli


Broccoli is a great source of glucosinolates, phytonutrients rich in sulfur that stimulate the natural antioxidant systems in your body. 

  • Barley


Like mushrooms, barley contains a high amount of beta glucans, known for their antioxidant and antimicrobial properties.


GoogleNews.com, September 1, 2009, by Aditi Justa  —  Harvesting solar power from space through orbiting solar farms sounds extremely interesting. Mitsubishi Electric Corp., a manufacturer of solar panels , has decided to join an AUD $25 billion Japanese project to construct a massive solar farm in space within three decades.

Japan has already started working towards achieving its goal by developing a technology for 1-gigawatt solar farm, which would include four square kilometers of solar panels that will be stationed 36,000 kilometers above the earth’s surface. The one gigawatt of energy that will be produced by the solar farm would be enough to supply power to nearly 294,000 average Tokyo homes.

Before the project is set to install, the Japan Aerospace Exploration Agency (JAXA), leaders of the project, will launch a small satellite consisting of solar panels in 2015. This launch will be to test beam energy from space. Working on these lines, the Institute of Space and Astronautical Science (ISAS), a division of JAXA has successfully designed a model of the SPS200, a 10-megawatt demonstration solar-power satellite. Apart from the satellite, ISAS is working on an experimental satellite plan that will provide wireless power supply of several hundred kilowatts.

A lot of experimentation is on in order to scrutinize the influence of high-voltage discharge necessary for large-capacity power generation in space and the impact of space debris.