LONGECITY

I mean, there are many compounds that alone, seems to somewhat reverse signs of aging.

 

quercertain, dasatinib

Pentoxifylline (tgf-b1 inhibitor)

 

Are they others ? 

You mention Pentoxifyline.  This is a book published last month on the drug:   http://www.barnesand..._-9781511673051

Title of the book is 

Pentoxifylline: A Versatile Off-Patent Medication Best Not Overlooked

Dear all,

 

I have passed the Longecity fundraiser details onto Dr Katcher who is interested in potentially working with us. He is currently discussing the project his with investors but advises he has an MD, physicians, a location and equipment and volunteers already arranged. From conversations I have had in the past with him the amount of plasma will be fairly substantial as he expressed concerns that the Alkahest project was not frequent enough to start reversing the age phenotype. Study size is only 1-2 people but hopefully we will get lots of useful data and a demonstration that the age phenotype can be reversed in people as it has in animal studies.

 

He is hoping to include Longecity in the project should the investors agree to it but it is very promising for the pilot study. I know we are interested in disruptive science and I am not sure I could think of anything more disruptive than this bar perhaps Gene therapy for TERT. He also has some ideas on how if proven effective we might get around the issue of Plasma supply to make the therapy more accessible which has me really curious.

 

I had a read of the project proposals and am I right in thinking if he put $10k into the project we could match that?

I'm not sure if 10k will help much the study, I think more is neede.

 

But we should do our best.

 

I believe are a lot of people that will donate if we will see clear results in humans.

 

Please post updates from Dr. Harold Katcher.

Radiation-induced enteropathy: Molecular basis of pentoxifylline–vitamin E anti-fibrotic effect involved TGF-β1cascade inhibition

 

 

http://www.thegreenj...0374-X/abstract

 

 

"The anti-fibrotic effect of combined pentoxifylline–vitamin E is at least in part mediated by inhibition of the TGF-β1 cascade."

 

 

its is more ptx + tocopherol that decrease tgf-b1, not ptx alone

Edited by Florian Xavier, 22 May 2015 - 04:54 PM.

Dear Alc et al,

I will keep you posted. I understand he has a number of investors interested so he may have access to more funds than 10k + 10k from Longecity should he be apply and get a project granted. I believe he may have a source of plasma organised and I suspect it might even be from volunteers so very fresh. He will need a fair amount based on what he has said about the amounts involved. If I can find out more I will update you.

 

 

 

 

Having spoke to Irina Conboy recently, TGF-beta looks key to rejuvenating stem cells. Judging by the papers I am reading it inhibits telomerase production thus leading to telomere shortening and the changes in gene expression that brings. Telomerase also promotes rejuvenation via the WNT pathway so if TGF-beta is inhibiting it the stem cell is going to be unable to work and heal tissue. So the answer? Inhibit TGF-Beta and reset telomeres for robust rejuvenation?

Regarding the photo of Catherine Deneuve vs Angela Merkel, it should read: 

 

Catherine Deneuve: once claimed to produce one interesting thought, although it wasn't recorded.

Angela Merkel: lead the 4th most powerful economy, reaching approval ratings of 77% and solving the euro-crisis.

a recent finding, connected to aging and the TGFbeta pathway:

 

miR-431 promotes differentiation and regeneration of old skeletal muscle by targeting Smad4
Lee & Shin et al. 2015 Aug 1

http://www.ncbi.nlm....pubmed/26215566

Abstract
The myogenic capacity of myoblasts decreases in skeletal muscle with age. In addition to environmental factors, intrinsic factors are important for maintaining the regenerative potential of muscle progenitor cells, but their identities are largely unknown. Here, comparative analysis of microRNA (miRNA) expression profiles in young and old myoblasts uncovered miR-431 as a novel miRNA showing markedly reduced abundance in aged myoblasts. Importantly, elevating miR-431 improved the myogenic capacity of old myoblasts, while inhibiting endogenous miR-431 lowered myogenesis. Bioinformatic and biochemical analyses revealed that miR-431 directly interacted with the 3' untranslated region (UTR) of Smad4 mRNA, which encodes one of the downstream effectors of TGF-ß signaling. In keeping with the low levels of miR-431 in old myoblasts, SMAD4 levels increased in this myoblast population. Interestingly, in an in vivo model of muscle regeneration following cardiotoxin injury, ectopic miR-431 injection greatly improved muscle regeneration and reduced SMAD4 levels. Consistent with the finding that the mouse miR-431 seed sequence in the Smad4 3' UTR is conserved in the human SMAD4 3' UTR, inhibition of miR-431 also repressed the myogenic capacity of human skeletal myoblasts. Taken together, our results suggest that the age-associated miR-431 plays a key role in maintaining the myogenic ability of skeletal muscle with age.

I support this experiment on an emotional level but unfortunately have no income would love to volunteer though

For TGF-beta studies check out the work by Irina and Michael who have demonstrated inhibiting it spurs rejuvenation in a number of tissues, it also reduces B2M levels and keeps them at more youthful profile once inhibited too, the Villeda lab identified B2M as another factor that impairs cognitive function in age. 

 

http://www.ncbi.nlm....les/PMC4494916/

 

This is the B2M study

 

https://www.ucsf.edu...system-molecule

 

However deal with TGF-b1 and the B2M problem goes away.