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DBL%20Hendrix%20small.png College chemistry, 1983

Derek Lowe The 2002 Model

Dbl%20new%20portrait%20B%26W.png After 10 years of blogging. . .

Derek Lowe, an Arkansan by birth, got his BA from Hendrix College and his PhD in organic chemistry from Duke before spending time in Germany on a Humboldt Fellowship on his post-doc. He's worked for several major pharmaceutical companies since 1989 on drug discovery projects against schizophrenia, Alzheimer's, diabetes, osteoporosis and other diseases. To contact Derek email him directly: derekb.lowe@gmail.com Twitter: Dereklowe

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In the Pipeline: Don't miss Derek Lowe's excellent commentary on drug discovery and the pharma industry in general at In the Pipeline

In the Pipeline

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March 17, 2010

BioTime's Cellular Aging Results

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Posted by Derek

A small company called BioTime has gotten a lot of attention in the last couple of days after a press release about cellular aging. To give you an idea of the company's language, here's a quote:


"Normal human cells were induced to reverse both the "clock" of differentiation (the process by which an embryonic stem cell becomes the many specialized differentiated cell types of the body), and the "clock" of cellular aging (telomere length)," BioTime reports. "As a result, aged differentiated cells became young stem cells capable of regeneration."

Hey, that sounds good to me. But when I read their paper in the journal Regenerative Medicine, it seems to be interesting work that's a long way from application. Briefly - and since I Am Not a Cell Biologist, it's going to be brief - what they're looking at is telomere length in various stem cell lines. Telomere length is famously correlated with cellular aging - below a certain length, senescence sets in and the cells don't divide any more.

What's become clear is that a number of "induced pluripotent" cell lines have rather short telomeres as compared to their embryonic stem cell counterparts. You can't just wave a wand and get back the whole embryonic phenotype; their odometers still show a lot of wear. The BioTime people induced in such cells a number of genes thought to help extend and maintain telomeres, in an attempt to roll things back. And they did have some success - but only by brute force.

The exact cocktail of genes you'd want to induce is still very much in doubt, for one thing. And in the cell line that they studied, five of their attempts quickly shed telomere length back to the starting levels. One of them, though, for reasons that are completely unclear, maintained a healthy telomere length over many cell divisions. So this, while a very interesting result, is still only that. It took place in one particular cell line, in ways that (so far) can't be controlled or predicted, and the practical differences between this one clone and other similar cells lines still aren't clear (although you'd certainly expect some). It's worthwhile early-stage research, absolutely - but not, to my mind, worth this.

Comments (4) + TrackBacks (0) | Category: Aging and Lifespan | Biological News | Business and Markets


COMMENTS

1. sgcox on March 17, 2010 8:37 AM writes...

Why is it such news ?
Better work has been done before by other group and published in a good jurnal:

http://dx.doi.org/10.1016/j.gde.2010.01.005

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2. anchor on March 17, 2010 8:54 AM writes...


Derek : There is a compelling reason/role for telomerase and other enzymes involved in the cell division. I am worried if these guys are going to end up creating cancer cells? Your comment please.

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3. John Harrold on March 17, 2010 10:46 AM writes...

Just out of curiosity, but are there folks out there in their younger years (20s or 30s) making attempts to preserve tissue samples under the assumption that when they hit their 80s or 90s they'll be able to use these preserved tissues in combination with current therapies of that time to reverse/counteract the effects of aging?

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4. RenegadeSci on March 17, 2010 9:55 PM writes...

They lost my interest when they mentioned the "telomere hypothesis of cellular aging".

If this was 2000, then i might read it.

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