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New cure for hair loss... in mice


#1

https://stemcell.ucla.edu/news/ucla-scientists-identify-new-way-activate-stem-cells-make-hair-grow


#2

Similar story here:

After having read articles like this over the years, I’ve become pretty jaded. Until they have a cure, I’m going to be skeptical.

http://newatlas.com/lactate-baldness/50893/


#3

If it is applied to the skin it shouldn’t be too difficult to test at home (if the cream is easy enough to find).


#4

It looks that more and more research indices show Jak involvement in hair growth.
What, if someone combined this with Treg cells?
Maybe we would not need Tsuji, Sisheido or Folica. Maybe answer is much simpler than DP, DSC, iPS or epithelial cells?


#5

This may just turn out to be the most significant discovery so far relating to the physiology of hair growth… If this holds up in humans, then any drug which safely increases lactate levels would be able to activate hair follicle stem cells. If follicles are still intact, this should (theoretically) lead to significant regrowth.


#6

Although definition of what is “follicle intact” and what is not, is very confusing thesedays, why do you need “follicle intact” in order for this theory to work? Do you imply that in case of “follicle is not intact” absence of Tregs would render lactate ineffective?


#7

I am skeptical as well regarding this. Otter’s point about the “follicle intact” variable is a very plausible one.

http://hairtransplanttestimonial.blogspot.com/


#8

Well, good question. The information I’ve read doesn’t specifically state anything about follicles having to be intact – that’s just something I wrote, based on common sense. In most people with MPB, the reason you don’t see terminal hairs growing is because the follicles have been miniaturized, and the stem cells are not being activated on a regular basis as they are in people without baldness. In the vast majority of cases, the follicles should still be there, in miniaturized form, and not destroyed or fibrosed. In a smaller percentage of cases, I would expect that the follicles have been damaged to the extent that they’re NOT intact.

So, please don’t read too much into what I wrote about the follicles having to be “INTACT”. It’s well-known that even most balding people still have intact follicles. Let’s not jump and make too much of this issue – which, after all, applies to ALL prospective treatments that attempt to rejuvenate dormant follicles.


#9

As to the connection between Tregs and lactate, I don’t think this has been established yet. It could be that in non-balding people, the regular appearance of Treg cells around the follicle send signals to regulate lactate dehodryogenase enzyme, which then activates the stem cells to proliferate and differentiate. What we’re looking at here is a multi-staged cycle with a lot of different steps.

The whole thing about lactate and pyruvate makes a lot of sense to me, though. Hair follicle growth requires a tremendous amount of concentrated energy. The UCLA research indicates that in normal skin cells, pyruvate gets shunted towards the mitochondria to create energy for the cells, but this doesn’t happen in hair follicle stem cells. In HFSCs, the “fuel” turns out to be lactate (also known as lactic acid). Interestingly, in striated muscle cells, after exercise, you make a lot of lactic acid, which causes muscle fatigue. It kind of makes sense to me, on a deep level, that the signaling for hair growth might involve lactate. The body compartmentalizes its functions, and a chemical that in one part of the body has one effect, might have a completely different effect in another part of the body. In your scalp, you have almost no striated muscle fibers, because people can’t move their scalps at will. So, it makes sense that lactic acid could have a completely different function there.


#10

So, if I’m getting this right. The second drug UK5099 blocks pyruvate from entering the mitochondria, thus making it to convert into lactate which activates hair follicle stem cells.
I don’t get it why they need the first drug RCGD423. They state that glucose in our bloodstream is the source of pyruvate metabolite production. And using UK5099 drug you convert it into lactate.
So perhaps eating more snickers would address the increase of glucose levels in our bloodstream, hence more pyruvate.

I found online plenty of suppliers of UK5099. It appears it is soluble in DMSO.
10mg $100 +.
Anyone willing to try? The cure might me sitting in front of our nose.


#11

@Otter I think both drugs independently increase lactate - they don’t have to be used together. As for Snickers, that will increase your glucose for sure, but won’t do a thing about the lactate in your HFSCs… Because in the pathology of MPB, no matter how much glucose is in your blood, almost none of it gets converted into lactate in and around the HFCS to matter. The problem is with the enzyme.