Cotsarelis/Garza Genetic analysis

[rdawg]

Cotsarelis' plan:

GPR44 blockers + supplementary pro-growth genes (eg PGE2)
If that doesn't work I believe there is already a way to "kick-start" the stem cells. Once the pdg2 effects are removed you would think they would function as normal again, but this is all TBC of course.

we're getting closer to figuring this out I can tell!

we may not have a cure in our hands in the near future but its comforting knowing that the understanding of it is getting much, much better!

[HairlossAt15]

Hey guys.

I wondered if one of us know how to contact dr. Cotsarelis, or his colleagues?
Maybe if we can get a hold and this guy ans his colleagus, we could get more info.

Greetings

AR

Hey, have you emailed him? and if so what did you ask and did he respond?

[HairlossAt15]

I don't think traditional growth promoters will cut it. Now that we have a better understanding, we need to focus on addressing the lack of progenitor cells. How to do it? Chemically? Culture cells in vitro?

Cotsarelis' plan:

GPR44 blockers + supplementary pro-growth genes (eg PGE2)
If that doesn't work I believe there is already a way to "kick-start" the stem cells. Once the pdg2 effects are removed you would think they would function as normal again, but this is all TBC of course.

[KO1]

I don't think traditional growth promoters will cut it. Now that we have a better understanding, we need to focus on addressing the lack of progenitor cells. How to do it? Chemically? Culture cells in vitro?

[rdawg]

The inhibition of PGD2 might slow down the process of hair loss but the prime question is will it have any cosmetic impact?

We need a treatment that is capable of regenerating hairs where there previously were none, the wound healing angle looks like a good one, but I'm more inclined right now to look at the work of Dr Gho and Dr Nigam in using the bodies own capabilities to induce donor regeneration, that's honestly our best shot right now.

Tough call but at least it sounds like we have some options in the near future.

It seems we do need a growth inducer along side a PGD2 inhibitor.

However PGD2 may be the next alternative to FIN, leaving out the side effects and doing a much better job of maintaining or maybe reinforcing the hair. But still with minimal regrowth.

PGD2 is intriguing though, but it definitely seems to be only one part of maybe a 2 or 3 part puzzle to regrow one's hair.(i.e PGD2 inhibition maintains the hair, stops hurting it+ FGF9 kick starts the follicles back to life + PGE2 helps to regrow those follicles).

[UK_]

So where can I get some PGD2 inhibitors?

The inhibition of PGD2 might slow down the process of hair loss but the prime question is will it have any cosmetic impact?

We need a treatment that is capable of regenerating hairs where there previously were none, the wound healing angle looks like a good one, but I'm more inclined right now to look at the work of Dr Gho and Dr Nigam in using the bodies own capabilities to induce donor regeneration, that's honestly our best shot right now.

[UK_]

But pgd2 directly inhibited hair growth on healthy(non-AGA) human hairs. Mice overexpressing pgd2 develop alopecia nothing is mentioned about whether or not they have high DHT levels or whether DHT has damaged them.

Yes this is what I mean, I personally feel that PGD2 is an inhibitor to the regenerative capabilities in the human body, it must down-regulate compounds such as FGF9 as it blocks certain receptor sites. As the hair follicle regenerates after every growth cycle, it's likely that PGD2 will interfere in this process of regeneration when applied even when there is no wound present.

[HairlossAt15]

Pgd2 is just a result of the damage caused to the follicle by DHT.

PGD2 is always present in the wound healing process during the latter stages while PGE2 is present during the initial stages.

They're not causes of hair loss, they're just present because androgens have damaged the hair follicle, I think it has more to do with the pathway to regeneration, PGD2 is somehow inhibiting the regeneration of the hair follicle after it has become damaged, this is why Dr Cots is looking at both the regeneration (FGF9) pathway and also the inhibition to regeneration (PGD2) pathway.

But pgd2 directly inhibited hair growth on healthy(non-AGA) human hairs. Mice overexpressing pgd2 develop alopecia nothing is mentioned about whether or not they have high DHT levels or whether DHT has damaged them.

[Boldy]

some sources that sell RU58841, have Crth2 inhibitors like OC000459, TM30089, or its weaker brother Ramatroban. the dose usually varies between 0.3% and 1%(3 mg per ml / 10 mg per ml). its still experimental.

there where 2 persons that did a foto log Cscot and babera:

http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=99747&STARTPAGE=62&FTVAR_FORUMVIEWTMP=Linear

[Boldy]

So where can I get some PGD2 inhibitors?

some sources that sell RU58841, have Crth2 inhibitors like OC000459, TM30089, or its weaker brother Ramatroban. the dose usually varies between 0.3% and 1%(3 mg per ml / 10 mg per ml). its still experimental.

[Boldy]

Originally Posted by Boldy
Its true that the dermal papilla over expresses androgen receptorss/ more sensitive for androgens. There it all starts. Pgd2 has huage impacts oh hair growth/ and proliferation of the cells.

in short, the pgd2 is responsible for androgen inducedDkk1(that is a WNT inhibitor), induces p53, tgfb, that triggers caspase apoptosis, and yet again dkk1, its and anti angiogenesis factor. Pge2|(the down regulated prostaglandin in AGA), is Pro angiogenesis, induces CD43+, wnt pathway, and FGF9.

this inbalance causes the hair to shrink, so not directly Androgens it self, but the triggered chain reaction behind it.

Check this topic for more detials: http://www.hairlosshelp.com/forums/m...hreadid=103373

Boldy

Im sorry but what does this mean?

(Ok here it is in normal human language)

Pgd2 is one of the big by products in the AGA follicles that disturbs the balance/ of proliferation/apoptosis of cells, for down regulation of growth factors, and it initiates apoptosis (cell death), and inhibition of progenitor cells. the other bad part in aga, is that the good for hairgrowth prostaglandin (PGE2), is 2x down-regulated.

Minox functions partly as a EP2 agonist, and its one(of the more) mechanisms why minox does work for hair loss!.


I think its more clear now?

[rdawg]

So where can I get some PGD2 inhibitors?

[ar50]

^PGD2 is really important and bad. Frankly a superior therapeutic target than simply antiandrogens.

SO its important for stopping hairloss And its bad for our health?

[KO1]

^PGD2 is really important and bad. Frankly a superior therapeutic target than simply antiandrogens.

[ar50]

Its true that the dermal papilla over expresses androgen receptorss/ more sensitive for androgens. There it all starts. Pgd2 has huage impacts oh hair growth/ and proliferation of the cells.

in short, the pgd2 is responsible for androgen inducedDkk1(that is a WNT inhibitor), induces p53, tgfb, that triggers caspase apoptosis, and yet again dkk1, its and anti angiogenesis factor. Pge2|(the down regulated prostaglandin in AGA), is Pro angiogenesis, induces CD43+, wnt pathway, and FGF9.

this inbalance causes the hair to shrink, so not directly Androgens it self, but the triggered chain reaction behind it.

Check this topic for more detials: http://www.hairlosshelp.com/forums/m...hreadid=103373

Boldy

Im sorry but what does this mean?