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[Mind]

Find out the latest MitoSENS news and discuss recent progress with Methuselah Foundation researcher Mark Hamlainen. This is the line of SENS research that received the huge donation from Peter Theil. The Sunday Evening Update is the only place you can get and in-depth interview with a cutting edge aging researchers such as Mark Hamalainen.

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[Mind]

Check out the new front page article as a refresher course on where we stand with regards to mitochondria and aging.

[Johan]

I have an exam on Monday, so I will not be able to tune in. However, I have a few questions which I would like to ask Mark Hamalainen:

In 2005, it was shown that mitochondrial protofection works in vivo in mice. Do you foresee any anti-aging therapies for humans based on this technology? Would it be possible to negate or significantly reduce the impact of mtDNA mutations by continually renewing the mtDNA using protofection?

Edited by Johan, 18 September 2008 - 05:33 PM.

[Mind]

Great question Johan. I would like to know not only if protofection will be tried in humans but when. I suspect since it is such a radical therapy it will take a long time for it to go through testing and be approved.

[AgeVivo]

MF thread concerning Mark's project: http://mfoundation.o...hread.php?t=111

[Mind]

Thanks for the link Agevivo!

If anyone has mitoSENS related questions, please bring them to the program, or ask them here in the thread so we can discuss them tomorrow.

[Mind]

from the MitoSENS page

The solution

As usual, we're lucky: evolution has done the hardest part of this for us already. Mitochondria are very complex; they contain about a thousand different kinds of protein, each encoded by a different gene. But nearly all of those genes are not in the mitochondrial DNA at all – they are in the nucleus! The proteins are constructed in the cell, outside the mitochondrion, just like all non-mitochondrial proteins. Then, a complicated apparatus called the TIM/TOM complex (no kidding...) hauls the proteins into the mitochondrion, through the membranes that make up its surface. Only 13 of the mitochondrion's component proteins are still encoded by its own DNA, and it’s therefore only these 13 genes that remain vulnerable to the constant assault from free radicals produced during respiration (the life-giving reaction of oxygen and food by the mitochondria).

This gives us a wonderful opportunity: rather than fixing mitochondrial mutations, we can make them harmless to us. By putting “backup copies” of these few remaining genes into the nucleus, we can prevent the harm caused by any mutations that may occur of the original versions. Even without the mitochondrial DNA, the proteins that it encodes will still be produced and incorporated into the mitochondrial machinery, allowing the cellular power plants to continue humming along normally. Doing this requires making a few minor modifications in the genes so that the proteins that they produce will be easier for the TIM/TOM machinery to handle, such as changing a few of the amino acid “building blocks” that make them up, or inserting disposable molecular “braces” called inteins into them that temporarily hold them straighter to keep them from getting tangled up as they cross the membranes. Since genes in our chromosomes are very, very much better protected from mutations than the mitochondrial DNA is, we can rely on the chromosomal copies carrying on working in very nearly all our cells for much longer than a currently normal lifetime.

[Mind]

Starting about 15 minutes from the time stamp of this post. Bring your questions.

[brokenportal]

Still going on, stop by and join in on the convo.

[Mind]

For those of you who did not attend you can watch later, however, you missed out on a nice treat. After the official recording ended Mark stayed around to participate in the text chat for a few extra minutes. Some past guests have done this as well.

Direct link to the video here

[Johan]

Does anyone have a log of the chat saved?