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Well then... at least we know it is a thing.
South Korean Scientists Has Developed A New Type Of Biochemical Material To Prevent Hair Loss
- Thread starter Xaser94
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Well then... at least we know it is a thing.
No, There is a conference in 2018 summer.
What's it called?
Interesting.
Here is the first patent which uses PTD-DBM for wound healing, it was filed in 2014 with a priority date of Feb that year.
https://www.google.com/patents/US9763994
They are purposefully very vague on the composition but there is some info in there. That means they've been using this stuff in experiments for at least 4 years.
https://www.google.com/patents/US9763994
They are purposefully very vague on the composition but there is some info in there. That means they've been using this stuff in experiments for at least 4 years.
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That reminds me something...
BMP antagonists: chordin, noggin, cerberus, follistatin.. already discussed here and there are studies showing their importance.
and they talk about noggin in the study.
Anyone? @InBeforeTheCure
BMP antagonists: chordin, noggin, cerberus, follistatin.. already discussed here and there are studies showing their importance.
and they talk about noggin in the study.
Anyone? @InBeforeTheCure
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Here's the problem: Different levels of CRTH2 signaling do affect response of hair follicles to PGD2, but they don't affect A.G.A risk. SNPs that dramatically reduce CRTH2 mRNA stability (reduces half-life by 2.67x or so) are highly associated with sensitivity of hair follicles to PGD2, but have zero effect on A.G.A as I explained here.
Compare that with pathological expansion of polyglutamine repeats (encoded by CAG repeats in DNA) in the Androgen Receptor (AR) in Kennedy's disease. Men with Kennedy's disease have something like 40-52 CAG repeats compared to the average 21-23 (source). 40-52 repeats reduces activation of AR target genes to around 75-85% that of the average (source). Men with Kennedy's disease have a reduced risk of A.G.A (source).
Here's another one: A famous missense mutation, rs3827760 T -> C (Val370Ala), in a gene critical for hair follicle development and cycling called EDAR (Ectodysplasin A Receptor). The mutation increases EDAR-mediated activation of NF-kB by about 1.5x (source). This mutation also reduces your chances of A.G.A. dramatically (odds ratio = 2) according to this study (Supplemental Data 9).
Well, hopefully you get the idea. Differences in the relative activities of certain genes/pathways that have some impact on causing a condition should affect chances of having that condition. If a large biological effect doesn't push the needle on someone's chances of having some biological trait, then logically that effect is unlikely to play much of a causative role. In other words, it's a symptom, not a cause.
VPA induces CXXC5 because it activates beta-catenin. Beta-catenin induces several negative feedback regulators (as well as positive feedback) - it's completely standard. For example, here's a short list from a study that profiled genes activated by Wnt3a in human dermal papilla cells.
Red are negative regulators of the Wnt pathway, green are positive regulators. Your question is like asking: "Dkk1 causes hair loss, so why is Wnt signaling not bad for hair?"
Here's a graph from the Lee study showing nuclear (i.e. activated) beta-catenin in mice treated with either nothing, PTD-DBM, VPA, or VPA + PTD-DBM respectively.
The VPA group is around 25%, the nothing group is around 10%. 25 > 10. That's why.
Anything in particular you want references for?
Which study?
Anyway, about Noggin, here are a few studies for you:
Generation of the primary hair follicle pattern - Mou et al.
Shh maintains dermal papilla identity and hair morphogenesis via a Noggin–Shh regulatory loop - Woo, Zhen, & Oro (possibly because BMP inhibits Edar expression as shown in the previous study, as well as in some microarray data that I have, and Shh is an Edar target gene)
Bone Morphogenetic Protein Signaling Regulates Postnatal Hair Follicle Differentiation and Cycling - Guha et al. (loss of hair with overexpression of Noggin - therefore, blasting hair follicles with BMP inhibitors 24/7 also not an option)
Are you studying Biochemistry or anything regarding medicine?
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Great work. Thanks for post. We might consider the possibility of hair cloning in conjunction with genetic modification as was recently done in cases of adrenoleukodystrophy. The prospect of potentially having any type of hair characteristic is exciting and will be possible. God knows when.
Can someone explain to me like I'm five years old why this find, if it amounts to any sort of treatment, would actually work?
Because as far as I can tell, it would do nothing to address the DHT problem (which mice do not have) and your follicles would still shrink regardless of using the compound.
As I recall, in-vitro experiments show that susceptible hair has the same negative reactions to the hormones.
The idea that we just have this protein binding to another and "inhibiting hair growth", which I read to mean "stops it cold turkey" in a very particular pattern is dubious at best.
Because as far as I can tell, it would do nothing to address the DHT problem (which mice do not have) and your follicles would still shrink regardless of using the compound.
As I recall, in-vitro experiments show that susceptible hair has the same negative reactions to the hormones.
The idea that we just have this protein binding to another and "inhibiting hair growth", which I read to mean "stops it cold turkey" in a very particular pattern is dubious at best.
it addresses the dht problem because cxxc5 activity is the mechanism by which dht inhibits hair growth/destroys follicles. therefore, by inhibiting cxxc5, you take dht out of the game, so to speak, and it is rendered essentially useless. think of dht as the messenger and cxxc5 as the message; by inhibiting the message (cxxc5), you spare the messenger (dht) and preserve follicles
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definitely. There are people who look to maintain without fighting dht itself. but others have to jump on anti dht .
so this is complicated, and hard to understand . there must be several reasons/factors. Maybe this discovery is the angle to look at ?who knows
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DHT / Prostaglandins / WNT/B-catenin pathway must all be related somehow, because otherwise, we wouldn’t see success of other people treating this condition through those different methods. We know that prostaglandins are attributed to anti inflammatory or inflammatory responses, and are directly related to circulation and bloodflow. I have a theory that the WNT pathway cannot function properly when there is chronic inflammation due to excessive PGD2. Can anyone shed some light on this? Does lack of circulation cause a disruption in the WNT pathway?
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Totally agree.
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You should look up DKK1.
Guys I have been following this thread since its beginning with being obsessed because this seems legit. Respected Dermatology Foundations referred to this study. Their study paper seems logical. We saw it in the news much more than the other treatments.
We find out from the study that a protein called CXXC5 is negative regulator of Wnt Pahtway which is important for hair growth and that they developed a compound called PTD-DBM. They are testing it on mice for toxicity.
So, Let's come to the point that I want to say. We don't know exactly if it will work on humans. In clincals %80 of the compounds don't work on humans. Therefore, We must make them aware of this study and encourage them to work on new CXXC5 inhibitors as alternative to PTD-DBM by contacting them.
I'm going to start by mailing the pharmatics in my country. So, I want your help. You can help me (also yourself) by contacting them about this.
Thanks
We find out from the study that a protein called CXXC5 is negative regulator of Wnt Pahtway which is important for hair growth and that they developed a compound called PTD-DBM. They are testing it on mice for toxicity.
So, Let's come to the point that I want to say. We don't know exactly if it will work on humans. In clincals %80 of the compounds don't work on humans. Therefore, We must make them aware of this study and encourage them to work on new CXXC5 inhibitors as alternative to PTD-DBM by contacting them.
I'm going to start by mailing the pharmatics in my country. So, I want your help. You can help me (also yourself) by contacting them about this.
Thanks