FROM TIME TO TIME, THIS BLOG DISCUSSES DISEASE PROCESSES. THE INTENTION OF THOSE DISCUSSIONS IS TO CONVEY CURRENT RESEARCH FINDINGS AND OPINIONS, NOT TO GIVE MEDICAL ADVICE. THE INFORMATION IN POSTS IN THIS BLOG IS NOT A SUBSTITUTE FOR A LICENSED PHYSICIAN’S MEDICAL ADVICE. IF ANY ADVICE, OPINIONS, OR INSTRUCTIONS HEREIN CONFLICT WITH THAT OF A TREATING LICENSED PHYSICIAN, DEFER TO THE OPINION OF THE PHYSICIAN. THIS INFORMATION IS INTENDED FOR PEOPLE IN GOOD HEALTH. IT IS THE READER’S RESPONSIBILITY TO KNOW HIS OR HER MEDICAL HISTORY AND ENSURE THAT ACTIONS OR SUPPLEMENTS HE OR SHE TAKES DO NOT CREATE AN ADVERSE REACTION.
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Meta
Yes. this is a needed one.
By the way here is another news
http://www.wired.com/wiredscience/2009/06/germlineimmortality/
Hi Vince
Here is another link on a ageless infant.
16 year old toddler who looks like 1 year old
http://io9.com/5302372/infant+sized-teenager-may-provide-key-to-reversing-the-aging-process
Thanks Res. I will follow through this afternoon. Nothing kike immirtakity to get me interested! Vince
Hi Res
Here is the text of the Nature abstract on roundworms:
“A soma-to-germline transformation in long-lived Caenorhabditis elegans mutants
Sean P. Curran1,2, Xiaoyun Wu1,2, Christian G. Riedel1,2 & Gary Ruvkun1,2
1.Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
2.Department of Genetics, Harvard Medical School, Boston, Massachusetts 02114, USA
Correspondence to: Gary Ruvkun1,2 Correspondence and requests for materials should be addressed to G.R. (Email: ruvkun@molbio.mgh.harvard.edu).
Unlike the soma, which ages during the lifespan of multicellular organisms, the germ line traces an essentially immortal lineage. Genomic instability in somatic cells increases with age, and this decline in somatic maintenance might be regulated to facilitate resource reallocation towards reproduction at the expense of cellular senescence. Here we show that Caenorhabditis elegans mutants with increased longevity exhibit a soma-to-germline transformation of gene expression programs normally limited to the germ line. Decreased insulin-like signalling causes the somatic misexpression of the germline-limited pie-1 and pgl family of genes in intestinal and ectodermal tissues. The forkhead boxO1A (FOXO) transcription factor DAF-16, the major transcriptional effector of insulin-like signalling, regulates pie-1 expression by directly binding to the pie-1 promoter. The somatic tissues of insulin-like mutants are more germline-like and protected from genotoxic stress. Gene inactivation of components of the cytosolic chaperonin complex that induce increased longevity also causes somatic misexpression of PGL-1. These results indicate that the acquisition of germline characteristics by the somatic cells of C. elegans mutants with increased longevity contributes to their increased health and survival.”
The key question for humans is whether we can reset our normal body cells to gene expression like in our germline cells insofar as genomic stability ois concerned without horrible things going wrong. Since we are a lot more complicated than roundworms that could be a challenge.
It is interesting that the worm researchers successfully messed around with the IGF-FOXO genetic pathway, the same one known to be involved in human longevity, that resveratrol impacts and that is being researched by Sirtris and others. My intuitive hunch is that it will be possible to discover epigenomic modifications that will take us a long way. This is a very interesting line of research.
Vince
Hi again res
The 16 year-old infant story is also interesting though it pushes my credulity since it reminds me of a PT Barnum sideshow exhibit. If the situation is real, it suggests that human physical developmental arrest may be possible – and could even contribute to longevity. Not exactly what I had in mind! It will be interesting to see if any real research results come out of the situation. Vince
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