Updated Research and Knowledge - Cutting Edge

[InBeforeTheCure]

For the Chr20 locus, the highest score was with rs6137444 (position chr20:21785638), the most upstream of the Chr20 SNPs associated with AGA: http://regulome.stanford.edu/snp/chr20/21785638

As you can see, it's around an AR binding site. It probably has nothing to do with FOXA2, since FOXA2 isn't expressed at all in hair follicles. It may affect PAX1, which is expressed in DP cells and which plays a role in pattern formation. Or maybe the culprit is the long non-coding RNA -- long non-coding RNA can have epigenetic roles. Of note:



So maybe androgen-dependent AR binding to this site slowly and permanently changes the epigenetic program of DPCs, which could be irreversible even with AR knockdown. Who the hell knows? It's fun to speculate.

It would be an interesting experiment if some researcher could see what happens when LINC01432 is overexpressed vs. underexpressed, what roles it may have, whether AR increases or decreases its expression in the presence or absence of DHT, and so on. And then maybe do the same with PAX1.

After looking around further, I think it's most likely PAX1. There are PAX1 enhancer regions downstream of PAX1.

A PAX1 enhancer locus is associated with susceptibility to idiopathic scoliosis in females

Idiopathic scoliosis (IS) is a common paediatric musculoskeletal disease that displays a strong female bias. By performing a genome-wide association study (GWAS) of 3,102 individuals, we identify significant associations with 20p11.22 SNPs for females (P=6.89 × 10−9) but not males (P=0.71). This association with IS is also found in independent female cohorts from the United States of America and Japan (overall P=2.15 × 10−10, OR=1.30 (rs6137473)). Unexpectedly, the 20p11.22 IS risk alleles were previously associated with protection from early-onset alopecia, another sexually dimorphic condition. The 174-kb associated locus is distal to PAX1, which encodes paired box 1, a transcription factor involved in spine development. We identify a sequence in the associated locus with enhancer activity in zebrafish somitic muscle and spinal cord, an activity that is abolished by IS-associated SNPs. We thus identify a sexually dimorphic IS susceptibility locus, and propose the first functionally defined candidate mutations in an enhancer that may regulate expression in specific spinal cells.

IS is a sexually dimorphic disease10. Girls and boys exhibit a striking difference in the prevalence of progressive IS, with girls having approximately tenfold greater risk of progressive curves that require operative treatment11. This dichotomy in female/male disease expression, and its correlation with the adolescent growth spurt have prompted investigations of hormonal influences in the development and progression of female IS6.

To discover new genetic risk factors for IS, we performed a two-stage GWAS in 3,102 individuals. Our results define a new susceptibility locus encoding associated SNPs that, surprisingly, are also associated with androgenic alopecia (AGA), or male pattern baldness. We find that the locus is specifically associated with female IS, suggesting that it contributes to the sexually dimorphic expression of the disease. By functional fine-mapping assays in zebrafish, we further define a sequence in the associated locus with enhancer activity that is abolished by IS-associated SNPs. Altogether, our results identify the first functionally characterized candidate mutations for IS susceptibility and expand our understanding of the role of non-coding regulatory elements in the disease. Our findings also suggest hypotheses to explain disease pathogenesis and provide the first insights into its puzzling sexual dimorphism.

Comparing our results to the National Human Genome Research Institute (NHGRI) GWAS catalogue22, we found that the chromosome 20 IS locus was previously associated with early-onset male pattern baldness (AGA). Similar to IS, AGA displays sexual dimorphism, that is, it is biologically unequal in males and females. However, unlike IS, disease progression in AGA (extent of hair loss) is generally more severe in males than in females36. We identified chromosome 20p11.22 SNPs that were previously associated with AGA and that were genotyped in our GWAS37, 38, 39. In this comparison, SNPs that were associated with IS and AGA displayed the opposite direction of effect for the two disorders (Supplementary Table 1). This observation suggested that sequences in the region conferring susceptibility to IS have a protective effect in AGA. To test whether the association we observed was sex-specific, we re-evaluated association with SNPs in the 20p11.22 locus after stratification by sex, that is, separating males and females. This analysis yielded evidence for association with IS in females but not males, with a combined Fisher’s P=6.88 × 10−9 in the former data set (Table 1 and Supplementary Tables 2 and 3).

Our investigation of the chromosome 20p11 locus provides the first genetic evidence to explain the puzzling sexual dimorphism that is a hallmark of IS. Besides susceptibility to progression, the pattern, onset and flexibility of deformity also differ between boys and girls10. Various hypotheses have been proposed to explain male/female differences in IS, including the existence of X-linked genetic risk factors and effects on circulating hormones. Neither mechanism has been clearly supported, although investigations have been limited6, 58. Our identification of a female-specific IS susceptibility locus suggests an underlying mechanism that is sensitive to the female milieu at the time of adolescence. Although we did not find evidence for oestrogen receptor-binding sites within the PEC7 enhancer locus itself, it is interesting to postulate that this locus increases risk of IS via downstream hormonal interactions. We note in this regard that the next-nearest gene, FOXA2, is implicated in sexually dimorphic gene expression via cooperation with androgen and oestrogen receptor59. It is possible that PEC7 regulates FOXA2. However, we did not detect Foxa2 expression in embryonic or postnatal mouse spine (data not shown) and consider it an unlikely candidate for IS susceptibility. PAX1 is also expressed in the adult scalp37. Whether variants in PEC7 affect this expression and drive association with early-onset male pattern baldness requires further study, but the overlapping genetic association suggests a possible correlation between the two sexually dimorphic conditions.

[burtandernie]

How important is it that we get some kind of AR antagonist like RU or CB that can compete with both T and DHT? It just seems like we desperately need another angle to fight androgens because raising T just seems stupid, and propecia has always felt like shooting a fly with a cannon by blowing up your endocrine system for a local problem

"ketoconazole cream 2% twice a day + finasteride + minox will cover the Androgen side if you've got good density or less aggressive AGA.

The problem with 5ar inhibitors, especially oral ones, is that they have a tendency to increase LH production and subsequently raise blood T levels and a local reduction in T's conversion to DHT leading to even more more T within cells. Suraphysical levels of T can activate the AR just as potently as DHT so it just offsets the potential gain from DHT inhibition. It's a tricky decision, yes Dut will kill more DHT, but you'll have even more T in comparison to Fin. I would stick to Fin."

[tiktok]

The problem with 5ar inhibitors, especially oral ones, is that they have a tendency to increase LH production and subsequently raise blood T levels and a local reduction in T's conversion to DHT leading to even more more T within cells.

That's not correct.

[joshuk]

can i mix oleuropein and VPA together in one vehicle or is it best to keep them seperate. Chemical the epi vpa had a light purple coating which i just peeled off and dissolved the powder into eth/pg

[musky]

Hydroxylation is the process by which 5ar gets converted to 3beta-diol. Keto and mico inhibit this step thus preventing the conversion of DHT to 3Beta-diol.

that's not what hydroxylation is and 5ar doesn't convert to 3beta-diol. 5ar converts testosterone to dht, dht is then converted by 3beta-hsd into 3beta-diol. 3beta-diol is then hydroxylated by some CP450 enzyme which i can't be bothered to research. it says that clearly in the abstract we keep posting back and forth to eachother.

[TheKingofFighters]

After looking around further, I think it's most likely PAX1. There are PAX1 enhancer regions downstream of PAX1.

A PAX1 enhancer locus is associated with susceptibility to idiopathic scoliosis in females

So tell me, because this is a critical question that i could not answer myself- whether do we need to INCREASE OR DECREASE PAX1's expression in the balding scalp(in order to regrow hair)?

Compounds that decrease PAX1:

Cacitriol(inhibits b-catenin)
Copper
Acetominophen(Panadol)
Bisphenol A(an estrogenic chemical)
Testosterone(androgenic hormone)

Compounds that increase PAX1:

Tretinoin(retinoic acid)
Valeric acid(present in anal cells of skunks)
Valproic acid(synthetic variant of Valeric acid)
Butyric acid(present in vomit)
Proprionic acid(present in sebum)
Ethinyl Estradiol(synthetic form of E2)
Curcumin
Resveratrol

[karxxx]

http://www.hairloss-research.org/LinkUpdateSawPalmettoandHairGrowthEffects1-14.html

https://www.google.si/patents/US7887694

http://www.hairloss-research.org/LinkUpdateAstaxantinDHT4-12.html

[TheKingofFighters]

So tell me, because this is a critical question that i could not answer myself- whether do we need to INCREASE OR DECREASE PAX1's expression in the balding scalp(in order to regrow hair)?

Compounds that decrease PAX1:

Cacitriol(inhibits b-catenin)
Copper
Acetominophen(Panadol)
Bisphenol A(an estrogenic chemical)
Testosterone(androgenic hormone)

Compounds that increase PAX1:

Tretinoin(retinoic acid)
Valeric acid(present in anal cells of skunks)
Valproic acid(synthetic variant of Valeric acid)
Butyric acid(present in vomit)
Proprionic acid(present in sebum)
Ethinyl Estradiol(synthetic form of E2)
Curcumin
Resveratrol

We present evidence of a new IS susceptibility locus in an ~100-kb region of chromosome 20p11.22 downstream of PAX1. Using a functional fine-mapping approach, we potentially narrow the locus to an ~1.5-kb domain with enhancer activity that is disrupted by disease-associated variants.(the IS-susceptible SNPs disrupts enhancer activity- presumably 'normal' activity for normal spinal development. We know from this study that these very same IS variants offers 'protection' from early onset baldness.) The PAX1-encoding region was originally associated with spinal development through studies of the naturally occurring undulated mouse strains. The original undulated (un) strain, first described in 1947, carries a missense mutation in Pax1 (ref. 41). Un/un mice display a curved spine with malformations of individual vertebrae including the vertebral bodies and intervertebral discs. Three additional strains, scoliosis (sco) or undulated intermediate (un-i), undulated-extensive (unex), undulated short-tail (uns), harbour partial or complete deletions of PAX1, with the latter including all of the gene and displaying the most severe phenotype41, 42.(A decrease/ablation in PAX1's expression confers malformations in the spine of rodents and amongst them- Scoliosis.) In early mouse development, Pax1 displays expression restricted to specific structures including the sclerotome that will give rise to the axial spine (vertebrae, ribs, connective tissues and skin). Genomic studies have delineated intervals downstream of Pax1 harbouring cis-regulatory activity consistent with this pattern43. In particular, transposon-based deletion mapping and reporter gene assays defined the ~148-kb region 3′ of Pax1 as necessary to drive somitic gene expression (that is, in the dorsal sclerotome) during early mouse development. Furthermore, the mouse Xe1 enhancer encoded in this region was shown to be sufficient to drive a similar expression pattern43. Our data using zebrafish transgene assays confirmed the enhancer activity of the human Xe1 orthologue and revealed another element in the region, PEC7, with potential somitic enhancer activity that was disrupted by IS-associated sequence variants.(The 'normal' variants in the affected region posseses potential somitic enhancer activity for proper spinal development, and is disrupted in those carrying the IS-associated variants.This observation strongly suggests that PEC7 itself functions in IS susceptibility, a hypothesis that may be tested in model systems by targeted mutagenesis.

All these implies that PAX1 needs to be DECREASED in order to regrow hair- because a decrease of PAX1 is what gives females a curved spine, but protection from hair loss.

But, im confused because PAX1 is involved with the profileration of stem cells

http://dev.biologists.org/content/141/4/737

So is it an INCREASE or DECREASE of PAX1(which is expressed in the adult scalp) to regrow hair?

Any1 who can answer this question accurately has basically- found the cure to AGA because in those who have carry no other AGA-susceptibility genes(e.g AR/EDAR, HDAC9, etc locus) other than the PAX1 variant- needs only to address this gene in order to regrow hair.

[Seuxin]

Hmmm Calcitriol is pretty cheap t get no ?
We just need to know an amount to test....

0.1%
1%

?

[mlamber5]

We present evidence of a new IS susceptibility locus in an ~100-kb region of chromosome 20p11.22 downstream of PAX1. Using a functional fine-mapping approach, we potentially narrow the locus to an ~1.5-kb domain with enhancer activity that is disrupted by disease-associated variants.(the IS-susceptible SNPs disrupts enhancer activity- presumably 'normal' activity for normal spinal development. We know from this study that these very same IS variants offers 'protection' from early onset baldness.) The PAX1-encoding region was originally associated with spinal development through studies of the naturally occurring undulated mouse strains. The original undulated (un) strain, first described in 1947, carries a missense mutation in Pax1 (ref. 41). Un/un mice display a curved spine with malformations of individual vertebrae including the vertebral bodies and intervertebral discs. Three additional strains, scoliosis (sco) or undulated intermediate (un-i), undulated-extensive (unex), undulated short-tail (uns), harbour partial or complete deletions of PAX1, with the latter including all of the gene and displaying the most severe phenotype41, 42.(A decrease/ablation in PAX1's expression confers malformations in the spine of rodents and amongst them- Scoliosis.) In early mouse development, Pax1 displays expression restricted to specific structures including the sclerotome that will give rise to the axial spine (vertebrae, ribs, connective tissues and skin). Genomic studies have delineated intervals downstream of Pax1 harbouring cis-regulatory activity consistent with this pattern43. In particular, transposon-based deletion mapping and reporter gene assays defined the ~148-kb region 3′ of Pax1 as necessary to drive somitic gene expression (that is, in the dorsal sclerotome) during early mouse development. Furthermore, the mouse Xe1 enhancer encoded in this region was shown to be sufficient to drive a similar expression pattern43. Our data using zebrafish transgene assays confirmed the enhancer activity of the human Xe1 orthologue and revealed another element in the region, PEC7, with potential somitic enhancer activity that was disrupted by IS-associated sequence variants.(The 'normal' variants in the affected region posseses potential somitic enhancer activity for proper spinal development, and is disrupted in those carrying the IS-associated variants.This observation strongly suggests that PEC7 itself functions in IS susceptibility, a hypothesis that may be tested in model systems by targeted mutagenesis.

All these implies that PAX1 needs to be DECREASED in order to regrow hair- because a decrease of PAX1 is what gives females a curved spine, but protection from hair loss.

But, im confused because PAX1 is involved with the profileration of stem cells

http://dev.biologists.org/content/141/4/737

So is it an INCREASE or DECREASE of PAX1(which is expressed in the adult scalp) to regrow hair?

Any1 who can answer this question accurately has basically- found the cure to AGA because in those who have carry no other AGA-susceptibility genes(e.g AR/EDAR, HDAC9, etc locus) other than the PAX1 variant- needs only to address this gene in order to regrow hair.

In my opinion this is the critical issue in AGA. What in the heck is going on at 20p11? Ar variants only confer greater risk to those of European heritage, it is monomorphic in Asians (existing in roughly only 1 type). 20p11 is by far the greatest at risk spot in asians, and is by a wide margin the second biggest risk point in Europeans. So it is the commonality between the two (along with androgenic hormones themselves... NOT androgen receptor.... only in europeans does this somehow accelerate the process).

http://www.hair-gel.net/

Although this is in mice, this is a highly useful website. In postnatal mouse skin, PAX1 is primarily expressed in the dermal papilla and in a smaller amount in the dermal fibroblasts. But I think we must be careful here on this. The set of SNP's at 20p11 are between PAX1 and FOXA2. The SNP's do lie closer to PAX1... But i'm not sure in which direction the DNA is being read on this strand... aka from PAX1 to FOXA2 or from FOXA2 to PAX1. That can make a big difference. Although FOXA2 is not expressed in postnatal mouse hair follicle environment, a quick look up of the functions of FOXA2 shows that IT HAS TO BE INVOLVED SOMEHOW IN AGA. FOXA2 is involved in ANDROGEN METABOLISM and response to IL-6... you can google these if you like for proof. IL-6 has been shown to be induced by DHT in AGA dermal papilla and it increases expression through p-STAT3 in the ORS and the bulge to induce premature Catagen. Stat3 is also present in dermal papilla and in other tissues has been known to up-regulates Ar gene expression and sensitivity to Androgenic hormones. So in my mind, even though FOXA2 isn't explicitly expressed in mouse postnatal hair follicle.... FOXA2 must be involved in some way in the parthenogenesis of AGA... There is still a lot we do not know about genetics especially when it comes to "junk" DNA (The DNA not directly involved in gene expression or protein coding.... It has a function science just isn't entirely sure how to read it yet). And that is exactly what we are dealing with at 20p11 and AR/EDA2R ( At risk SNP's are between genetic coding on "junk" DNA ).

[mlamber5]

And secondly the only way to really attack this in the near term (before CRISPR and like-systems) is to find out what proteins/pathways are being activated and silencing them or up-regulate them. I could fill the next 30 posts with articles and information to explain... the information is free for all to research and draw their own conclusions on the internet but in my mind AGA comes down to 4 main factors in people of European ancestry. The first is Androgenic hormones themselves. The second is the Androgen receptor. The third is overexpressed STAT3/PStat3, especially as it relates to the bulge and dermal papilla. And finally the fourth is the cytokine Interleukin-6, which is pro-inflammatory and works mainly through the JAK/STAT3 pathway. It is the interplay of these four which I think is causing the entire phenotype we see in AGA, and the correlation/association between other at risk factors in those that have AGA such as BPH, Diabetes, Prostate Cancer, Parkinson's Disease, and much greater risk of idiopathic scoliosis in females (another 20p11 major at risk spot). Stoping Ar itself will merely slow down the progression of AGA. The only way we know of so far to stop it dead in its tracks is castration, and that obviously isn't an option. I think the combination of a topical JAK/STAT inhibitor and an androgen suppressor at the same time (such as finasteride ) could potentially cause GREAT reversal in AGA phenotype.

[TheKingofFighters]

[q] I think the combination of a topical JAK/STAT inhibitor and an androgen suppressor at the same time (such as finasteride ) could potentially cause GREAT reversal in AGA phenotype. [/q]

On the Contrary- i do not think so.

[InBeforeTheCure]

So tell me, because this is a critical question that i could not answer myself- whether do we need to INCREASE OR DECREASE PAX1's expression in the balding scalp(in order to regrow hair)?

Compounds that decrease PAX1:

Cacitriol(inhibits b-catenin)
Copper
Acetominophen(Panadol)
Bisphenol A(an estrogenic chemical)
Testosterone(androgenic hormone)

That's interesting that testosterone is known to decrease PAX1. In what context, and can you give us a source? That region just downstream of PAX1/FOXA2 (which is from about 21.5 Mb to 22.5 Mb) is loaded with androgen response elements (AREs):



(Bolton et. al, 2007, supplementary material)

Perhaps AR binds to that region and affects chromatin structure. Then the SNPs in between the AR binding site and PAX1 might alter an insulator sequence that stops those chromatin changes from propagating to PAX1. The effect could be either to prevent it from being upregulated (enhancer blocking element) or to prevent it from being downregulated (barrier element).

By the way, that exact same region between PAX1 and FOXA2 has showed up again in GWAS, this time in association with nose width. This was published just a couple weeks ago: http://www.nature.com/ncomms/2016/16...omms11616.html

Strongest association in 20p11 with the ordinal assessment of nose wing breadth was observed for SNP rs927833 located in LOC100270679, a long intergenic non-protein coding RNA (LINC01432). There is substantial LD around this SNP and suggestive evidence of association (that is, P values <10−5), for SNPs over a region of ~400 kb extending to the Paired-box gene 1 (PAX1; Fig. 3f), a strong candidate gene in this region. PAX1 is a key developmental transcription factor which has been shown experimentally to affect chondrocyte differentiation through its participation in a regulatory pathway that also includes RUNX2 and SOX9 (ref. 46). More broadly, a Pax-Six-Eya-Dach (Dachshund) network, involving protein–protein and protein–DNA interactions impacting on a range of basic developmental processes has been described47. As indicated above, another PAX gene (PAX3) has been twice reported to impact on nasion position9, 11, and we replicate that association here. A missense mutation in PAX1 has been shown to cause autosomal recessive oto-facio-cervical syndrome, a disorder characterized by various skeletal and facial abnormalities48. It has also been reported that mouse embryos with Gli3-null mutations display drastically reduced Pax1 expression, possibly mediated through Gli3’s involvement in the sonic hedgehog signalling pathway49. Consistent with these experimental findings, we observe a significant statistical interaction of the GLI3 and PAX1 index SNPs on nose wing breadth (P value=0.005, Supplementary Table 17).

So perhaps if someone were to look at it, they would find some correlation between nose width breadth and baldness because of this.

Anyway, since PAX genes are responsive to hedgehog signaling, I wonder if PAX1 does its damage (or protects from it) in early anagen, when transit amplifying cells are hitting the dermal papilla cells with Shh.

All these implies that PAX1 needs to be DECREASED in order to regrow hair- because a decrease of PAX1 is what gives females a curved spine, but protection from hair loss.

But, im confused because PAX1 is involved with the profileration of stem cells

http://dev.biologists.org/content/141/4/737

It's hard to say which way it might go, since for example MAPT is upregulated in Parkinson's disease but downregulated in AGA DPCs even though the SNPs associated with AGA are the same ones associated with Parkinson's. These elements interact in complex networks, so a change that might affect things one way in one context might affect things the opposite way in another. So who knows? The difference in expression might only be transient too, such as embryonic or at one part of the hair cycle (like early anagen).

So is it an INCREASE or DECREASE of PAX1(which is expressed in the adult scalp) to regrow hair?

Any1 who can answer this question accurately has basically- found the cure to AGA because in those who have carry no other AGA-susceptibility genes(e.g AR/EDAR, HDAC9, etc locus) other than the PAX1 variant- needs only to address this gene in order to regrow hair.

Not necessarily. It could be that the process is similar in everyone, but the genes that show up in GWAS are like "resistance points" in the network that prevent the process from occurring or alters the speed at which it occurs, but once it gets enough momentum it snowballs.

In my opinion this is the critical issue in AGA. What in the heck is going on at 20p11? Ar variants only confer greater risk to those of European heritage, it is monomorphic in Asians (existing in roughly only 1 type). 20p11 is by far the greatest at risk spot in asians, and is by a wide margin the second biggest risk point in Europeans. So it is the commonality between the two (along with androgenic hormones themselves... NOT androgen receptor.... only in europeans does this somehow accelerate the process).

http://www.hair-gel.net/

Yeah, I love Rendl's site. And if you haven't seen it, here's the paper that goes along with the postnatal stuff: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826467/

Although this is in mice, this is a highly useful website. In postnatal mouse skin, PAX1 is primarily expressed in the dermal papilla and in a smaller amount in the dermal fibroblasts. But I think we must be careful here on this. The set of SNP's at 20p11 are between PAX1 and FOXA2. The SNP's do lie closer to PAX1... But i'm not sure in which direction the DNA is being read on this strand... aka from PAX1 to FOXA2 or from FOXA2 to PAX1. That can make a big difference. Although FOXA2 is not expressed in postnatal mouse hair follicle environment, a quick look up of the functions of FOXA2 shows that IT HAS TO BE INVOLVED SOMEHOW IN AGA. FOXA2 is involved in ANDROGEN METABOLISM and response to IL-6... you can google these if you like for proof. IL-6 has been shown to be induced by DHT in AGA dermal papilla and it increases expression through p-STAT3 in the ORS and the bulge to induce premature Catagen. Stat3 is also present in dermal papilla and in other tissues has been known to up-regulates Ar gene expression and sensitivity to Androgenic hormones. So in my mind, even though FOXA2 isn't explicitly expressed in mouse postnatal hair follicle.... FOXA2 must be involved in some way in the parthenogenesis of AGA... There is still a lot we do not know about genetics especially when it comes to "junk" DNA (The DNA not directly involved in gene expression or protein coding.... It has a function science just isn't entirely sure how to read it yet). And that is exactly what we are dealing with at 20p11 and AR/EDA2R ( At risk SNP's are between genetic coding on "junk" DNA ).

I posted a paper earlier in this thread about non-coding RNA functions, but I'll post it here again: http://genesdev.cshlp.org/content/23/13/1494.full.html

However, those regions are probably regulatory regions for nearby genes for the most part. But non-coding RNAs could be playing a role even in that.

And secondly the only way to really attack this in the near term (before CRISPR and like-systems) is to find out what proteins/pathways are being activated and silencing them or up-regulate them.

I agree completely, and for the past few weeks I've been working on a hypothesis as to how this thing could work. It's an incomplete model, and only experiment can say whether it's true or not true or partially true, but nevertheless I'll be posting a thread on that sometime in June. I've got the main idea, but I want to do a couple things first -- first I'm going to a bioinformatics analysis, and then I want look at mesenchymal-epithelial interactions more closely as well.

[mlamber5]

[q] I think the combination of a topical JAK/STAT inhibitor and an androgen suppressor at the same time (such as finasteride ) could potentially cause GREAT reversal in AGA phenotype. [/q]

On the Contrary- i do not think so.

Thanks for your contribution

[mlamber5]

Looking forward to it. I can see we both have started from the same point, the genes it looks like. If indeed JAK/STAT inhibition does end up reversing AGA it would only make sense that the team that discovered the key pieces of information and cure to hair loss ( Christiano's team ) is a team that focuses on the genetics behind all types of hair loss.