Manipulating Mitochondria

The more work being done to tinker with our mitochondria, the power plants of our cells, the better. A growing, well-funded research and development community focused on mitochondrial engineering is a necessary step on the road to robust repair technologies that can remove or work around the mitochondrial damage that contributes to aging.

My attention was drawn today to the latest example of mitochondrial engineering:

the protein, rhTFAM (an abbreviation for recombinant-human mitochondrial transcription factor A), succeeded in entering and energizing the DNA of the mice’s mitochondria, enabling them to run two times longer on their rotating rods than a control group cohort.

Because many neurodegenerative diseases cause mitochondria to malfunction, medical researchers have been focusing on developing methods for repairing and restoring them. The new UVA study represents an important step toward achieving that goal. It shows that a naturally occurring protein, TFAM, can be engineered to rapidly pass through cell membranes and target mitochondria. Study findings show that rhTFAM acts on cultured cells carrying a mitochondrial DNA disease as well as lab mice.


Mitochondria are the cellular engines that transform food into fuel in our bodies and perform their work in the energy-intensive tissue of our brains, retinas, hearts and skeletal muscles. When damaged, mitochondria slow down, stop generating energy effectively and begin to over-produce oxygen free radicals. If produced in excess, oxygen free radicals chemically attack all cell components, including proteins, DNA and lipids in cell membranes.

"In simple terms, an overabundance of these free radicals cause cells to start rusting," notes lead study author James P. Bennett, Jr., M.D., PhD, a professor of neurology and psychiatric research at the UVA School of Medicine and director of its Center for the Study of Neurodegenerative Diseases.

While the UVA findings are preliminary, Bennett considers them encouraging. "We've shown that the human mitochondrial genome can be manipulated from outside the cell to change expression and increase mitochondrial energy production," he notes. "This is arguably the most essential physiological role of the mitochondria."

This particular research likely has little impact on the issue of mitochondrial damage and aging, but it is encouraging to see a breadth of work taking place in areas that will provide support to developing methods of repair for our mitochondria.


Consider sending something like this to YOUR congressman & senators:

Thank you for your work on the stimulus plan. Today the markets are the biggest challenge to our economy. Looking forward, spending will be our greatest problem, in particular Social Security and Medicare. Republicans would eliminate them, if they could. Democrats would tax more to try to make them solvent. Most Americans want neither solution.
The alternative solution requires rethinking demographics, and some scientific investment.
The reason 65 was the age set for retirement during the New Deal was because most workers died before 64 in the 1920’s. Life was harder. Most jobs involved heavy physical labor. Healthcare was poorer.
Today’s entitlement problem is not a financial problem. It’s a demographics problem. Today’s average life expectancy is 78 and rising. Healthcare’s better. Work’s less strenuous. But most Americans resist retiring at 78 because they believe old age will rob them of the strength to work that long. But as more retirees are supported by fewer workers, the system will fail.
The alternative is to cure the diseases of old age so people can work at 80 as though they were 60 again. Much work has been started on this, but a concerted effort to finish it is needed now to make a difference in solving the coming entitlement crisis.
Below is a partial list of people working on the problem.
With enough government support, a sustained scientific effort, like that of the space program, could yield substantial benefits before the worst of the demographic pressures hit. Pooling and coordinating the effort in one place, perhaps UVA or Virginia Tech, will provide a focus for information services to persuade an aging work force that working longer and maintaining a good quality of life are compatible.
Ciao e Buona Fortuna,

Gary AndrewS

-Cynthia Kenyon, Hillblom Center for the biology of Aging, San Francisco
-David Scaddon, M.D. & Anthony Komaroff, M.D., Harvard Medical School
-Brian Kennedy & Matt Kaeberlain, University of Washington, Seattle
-T. Keith Blackwell, Harvard Medical School
-Nir Barzilai, Institute for Aging, Albert Einstein College of Medicine, NY,NY
-Thomas Rando, Stanford University
-D. Leanne Jones, Salk Institute for Biological Studies, La Jolla, CA
-Norman Sharpless, University of North Carolina, Chapel Hill
-Woodring Wright, University of Texas Southwestern Medical Center, Dallas
-Hemachandra Reddy, Oregon Health & Science University, Beaverton
-Mark Mattson, National Institute on Aging, Baltimore

Posted by: Gary AndrewS at April 14th, 2009 4:50 AM

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