Dr. Angela Christiano - Bernstein Medical - Center for Hair Restoration
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Two new studies researching a class of drugs called JAK inhibitors have shown that oral treatment results in significant hair regrowth in patients with alopecia areata, an autoimmune condition that causes non-scarring patches of localized hair loss. Currently there is no cure for alopecia areata, so the possibility of a safe, effective medication is welcome news for thousands of affected patients.

Background

Last year we wrote about how the two new FDA-approved drugs tofacitinib and ruxolitinib act as inhibitors of the family of enzymes called Janus kinase (JAK). ((Harel S, Higgins CA, Cerise JE, Dai Z, Chen JC, Clynes R, Christiano AM. Pharmacologic inhibition of JAK-STAT signaling promotes hair growth. Sci Adv. 2015 Oct; 1(9): e1500973.)) By inhibiting the JAK enzymes, the drugs disrupt intracellular communication to white blood cells, called “T lymphocytes,” and are thus useful in treating alopecia areata. The JAK inhibitors prevented the onset of the disease and reversed the condition, enabling hair to regrow in areas previously devoid of hair.

The 2015 study we referenced – led by renowned alopecia areata researcher Dr. Angela Christiano – showed that topical application of tofacitinib and ruxolitinib in mice resulted in the rapid transition of hair follicles from the telogen (resting) phase of the hair cycle to the anagen (growth) phase. The same study found that tofacitinib encouraged hair follicle development in clumped human dermal papilla (DP) cells, stem cells that are critical in the development of hair follicles. [1]

The Studies

The two new studies were published in September 2016 in the journal JCI Insight, a peer-reviewed journal dedicated to biomedical research.

Tofacitinib

The study of oral tofacitinib – by Crispin, Ko, et al – was a 2-center, open-label, single-arm trial; the first to systematically examine the efficacy of JAK inhibitors as a treatment for alopecia areata. ((Crispin MK, Ko J, Craiglow BG, Li S, Shankar G, Urban JR, Chen JC, Cerise JE, Jabbari A, Winge MG, Marinkovich MP, Christiano AM, Oro AE, King BA. Safety and efficacy of the JAK inhibitor tofacitinib citrate in patients with alopecia areata. JCI Insight. 2016;1(15):e89776. doi:10.1172/jci.insight.89776.)) In addition to studying alopecia areata (AA) patients with greater than 50% scalp hair loss, they tested the drug on patients with alopecia totalis (AT), which is the complete loss of scalp hair; alopecia universalis (AU), the loss of scalp and body hair; and ophiasis pattern alopecia areata, hair loss localized to the temporal and occipital scalp. After three months on 5mg tofacitinib citrate, 32% showed up to 50% improvement, and 32% showed greater than 50% improvement. When broken down by subtype of the condition, those with AA improved by 70% on average, those with ophiasis improved by 68%, AT by 11.8%, and AU by 10.5%. They found that following cessation of the treatment, all patients experienced a recurrence of hair loss after an average of 8.5 weeks. Additional trials are necessary to determine the optimal dosage regimen for providing the most long-lasting response.

Ruxolitinib

The study of ruxolitinib – by Mackay-Wiggan, Jabbari, et al – was an open-label clinical trial of 12 patients with moderate to severe alopecia areata. ((Mackay-Wiggan J, Jabbari A, Nguyen N, Cerise J, Clark C, Ulerio G, Furniss M, Vaughan R, Christiano AM, Clynes R. Oral ruxolitinib induces hair regrowth in patients with moderate-to-severe alopecia areata. JCI Insight. 2016;1(15):e89790. doi:10.1172/jci.insight.89790.)) The pilot study tested the use of 20mg oral ruxolitinib twice a day for three to six months; this was followed by three months of monitoring the patients without treatment. Despite the small sample size, the results were striking in that 75% of patients showed a strong response to the medication, with hair regrowth over 50%. After treatment, those who responded to the treatment exhibited a 92% reduction in hair loss. Seven of the nine responders achieved greater than 95% hair regrowth. After stopping treatment hair loss resumed; however, it did not reach the level of hair loss that was present before treatment. This proof-of-concept pilot study showed that ruxolitinib is a safe and effective in reversing the balding effects of alopecia areata.

Conclusion

After showing promise in previous research, scientists have now shown that JAK inhibitors have strong potential to cause substantial hair regrowth in people with alopecia areata; a condition that causes hair loss that can be socially awkward at best and cosmetically disfiguring in severe cases. More studies need to go forward in order to determine which of the two drugs – tofacitinib or ruxolitinib – will be the most effective treatment, and what the proper dosage is for long-term treatment. However, we are hopeful that a medication will be developed for broad use in treating alopecia areata patients.

The other major point of interest following the publication of the series of studies is the potential for JAK inhibitors to treat androgenetic alopecia, or common genetic hair loss. One area that is being discussed is the potential for JAK inhibitors, perhaps in the form of a topical treatment, to stimulate the transition of hair follicles from the resting phase to the growth phase of the hair cycle. Christiano’s research is examining the effects of JAK inhibitors on cultured dermal papilla (DP) spheres. If JAK inhibitors can be used to stimulate DP spheres to grow into mature hair follicles, it may enable hair multiplication techniques to become a viable treatment for common baldness.

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Dr. Angela Christiano and her team of researchers at Columbia University studying the autoimmune disease alopecia areata, have shed new light on how to move hair follicles from their resting stage (telogen) into the growth stage (anagen) in which they can produce normal hairs. The study, published in the October issue of Science Advances, introduces the possibility of a new topical medication for hair growth stemming from a class of chemicals that block enzymes in the Janus kinase (JAK) family. ((Harel S, Higgins CA, Cerise JE, Dai Z, Chen JC, Clynes R, Christiano AM. Pharmacologic inhibition of JAK-STAT signaling promotes hair growth. Sci Adv. 2015 Oct; 1(9): e1500973.)) The findings on the topical application of JAK inhibitors have implications in the treatment of common hair loss as well as alopecia areata, which causes a non-scarring form of localized hair loss.

Scientists had, until now, tried unsuccessfully to use drugs to induce follicles en masse into the anagen phase. The two FDA-approved medications currently used to treat hair loss each use a different approach. Finasteride (Propecia) blocks the conversion of testosterone to dihydrotestosterone (DHT) – the hormone that causes genetically susceptible hair follicles to progressively shrink or miniaturize. Minoxidil (Rogaine) extends the anagen phase, thereby delaying the onset of hair follicle miniaturization. JAK inhibitors could develop into a third major medical option for the treatment of hair loss.

Background: Research Investigating Alopecia Areata

Dr. Christiano, herself diagnosed with alopecia areata, has made several significant breakthroughs involving hair loss and its treatment in the past. Bernstein Medical has written extensively about her study of alopecia areata, hair loss genetics, and hair cloning.

Building on initial research in 1998 implicating a type of white blood cell known as “T lymphocytes” in the development of alopecia areata, ((Gilhar A, Ullmann Y, Berkutzki T, Assy B, Kalish RS. Autoimmune hair loss (alopecia areata) transferred by T lymphocytes to human scalp explants on SCID mice. J Clin Invest. 1998 Jan 1; 101(1):62-7.)) Dr. Christiano and her team set out to find ways to modulate them. In research published in the September 2014 issue of Nature Medicine, they looked at two different FDA-approved chemicals, ruxolitinib and tofacitinib, and how they act as inhibitors of enzymes in the family Janus kinase (JAK). Inhibiting JAK cut off communication to the T cells. Without an accumulation of T cells, alopecia areata could not progress. ((Xing L, Dai Z, Jabbari A, Cerise JE, Higgins CA, Gong W, de Jong A, Harel S, DeStefano GM, Rothman L, Singh P, Petukhova L, Mackay-Wiggan J, Christiano AM, Clynes R. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nat Med. 2014 Sep; 20(9):1043-9.)) The JAK inhibitors both prevented the onset of the disease, and reversed the condition where it was already established.

The most surprising finding of this study concerned the effect of topically applying the inhibitors.

“We found that topical ruxolitinib and topical tofacitinib were both highly effective in reversing disease in treated lesions (applied to back skin). A full coat of hair emerged in the ruxolitinib- or tofacitinib-treated mice by 7 weeks of treatment, and we observed complete hair regrowth within 12 weeks following topical therapy.”2

Findings: JAK Inhibitors and Hair Growth in Normal Subjects

Having successfully tested JAK inhibitors against alopecia areata, Dr. Christiano and her team sought to investigate JAK inhibition on normal mice and humans.

The researchers applied solutions of tofacitinib and ruxolitinib to one side of the backs of mice with hair in the telogen phase, while the other side was treated with a control solution. Within seven days of treatment, each mouse saw robust hair growth on the treated side, while the control side did not. This indicates a rapid transition of the hair cycle from telogen (resting) to anagen (growth). Furthermore, they found that treatment with JAK inhibitors resulted in “significant proliferation” of hair follicle stem cells, indicating that the inhibitors activated progenitor stem cells within the follicles. The topical application of JAK inhibitors in mice unmistakably resulted in rapid onset of hair growth.

Next, the team looked at the effects of JAK inhibitors on cultured dermal papilla (DP) spheres. In 2013, Dr. Christiano achieved a breakthrough in using an ingenious technique, called a “hanging drop culture.” Using this process, her team caused dermal papilla cells to clump together in a spherical (tear drop) shaped configuration. They found that DP cells in this three-dimensional mass more easily communicate with one another and are then capable of forming new hair follicles. When cultured in a solution containing the JAK inhibitor, tofacitnib, the DP spheres showed an enhanced ability to induce hair follicle development in larger sizes and in significantly greater numbers.

Conclusion/Summary

Topical application of JAK inhibitors leads to the activation and proliferation of hair follicle stem cells and a rapid transition to the anagen phase of the hair growth cycle. This research could be the catalyst for the development of a new topical treatment for hair loss that could potentially benefit individuals who are not indicated for, or who have not seen a positive response from, traditional hair loss medications or are not candidates for hair transplantation. Additionally, JAK inhibitors may be developed into a topical treatment for alopecia areata and potentially other autoimmune conditions that cause localized hair loss or other skin problems. JAK inhibitors might even aid in the development of hair cloning techniques, which could effectively cure hair loss.

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Could a hormone that plays a critical role in red blood cell production also play a critical role in hair follicle production? According to a 2010 research report published in the Journal of Dermatological Science, this may be the case.

Erythropoietin Implicated In Hair Growth Regulation

The hormone in question is called Erythropoietin (EPO). It is produced in the kidneys in order to regulate red blood cell production. Recent studies have shown that EPO is also produced in a structure that surrounds and protects a hair follicle, the outer root sheath (ORS). Moreover, other studies have found that the EOP secreted by the ORS seems to target dermal papilla (DP) cells. DP cells play a critical role in regulating hair growth.

Because of these results, researchers have speculated that EPO may affect hair growth by acting on DP cells, but no direct evidence for this had ever been found – until now.

Evidence That EPO Affects Hair Growth in Vitro (Cell Cultures)

Strong evidence of EPO’s direct involvement in hair growth would be the discovery of EPO receptor sites (EPOR) on DP cells and a clear mechanism of how EPO affects changes in a DP cell (called cell signaling); this is exactly what researchers in the Republic of Korea ((Kang BM, Shin SH, Kwack MH, Shin H, Oh JW, Kim J, Moon C, Moon C, Kim JC, Kim MK, Sung YK. Erythropoietin promotes hair shaft growth in cultured human hair follicles and modulates hair growth in mice. J Dermatol Sci. 2010 Aug;59(2):86-90. doi: 10.1016/j.jdermsci.2010.04.015. Epub 2010 May 19.)) have found. Not only did they find direct evidence of EPO receptive sites but they also discovered the critical cell signaling mechanism: phosphorylated EPOR signaling pathway mediators.

In addition to discovering the signaling mechanism, they also showed using cell cultures that EPO causes both dermal papilla to proliferate and hair shafts of human hair follicles to elongate.

While the effects of EPO on DP and hair follicles were compelling, they only occurred in vitro (in cell cultures outside the body) and it is known that cells cultured on a flat surface behave significantly differently than cells that exist in situ, inside the organism (see Higgins and Christiano, Regenerative Medicine And Hair Loss: How Hair Follicle Culture Has Advanced Our Understanding Of Treatment Options For Androgenetic Alopecia).

Evidence That EPO Affects Hair Growth In Situ (In The Body)

In order to better answer the questions of whether and how EPO might directly affect hair growth in situ, the Korean researchers implanted EPO treated DP cells into mice and found that these treated cells not only moved hair follicles from their resting (telogen) phase into an active hair growth (anagen) phase but also prolonged a follicle’s active growth phase.

This is a significant finding since one of the mechanisms of male pattern baldness is DHT susceptible hair follicles entering into progressively longer periods of a telogen (resting) phase relative to an anagen (hair growth) phase. EPO, having the opposite effect on hair follicles, opens the door to treating this type of hair loss with existing EPO analogs and/or developing new erythropoietin biopharmaceuticals.

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Progress towards hair cloning may have just have shifted up another gear thanks to scientists at the University of Pennsylvania and the New Jersey Institute of Technology. The breakthrough study published January 28th, 2014 is the first to show the successful transformation of adult human skin cells into quantities of epithelial stem cells necessary for hair regeneration.

The researchers, led by Dr. Xiaowei “George” Xu, started with human skin cells called dermal fibroblasts, then transformed those into a type of stem cell called induced pluripotent stem cells (iPSCs). These were then transformed into epithelial stem cells (EpSCs). This important step had never been achieved before in either humans or mice. The epithelial stem cells were combined with mouse dermal cells, that can be induced to form hair follicles, and then grafted on a mouse host. The epithelial cells and dermal cells then grew to form a functional human epidermis and follicles structurally similar to human hair follicles. The exhibits that accompany the study include photographic evidence of human hairs.

Figure 5 - Generation of folliculogenic human epithelial stem cells from induced pluripotent stem cellsHair shafts (arrowheads) formed by induced pluripotent stem cell-derived epithelial stem cells compared to mouse hair (arrows). — Credit: Ruifeng Yang, Perelman School of Medicine, University of Pennsylvania

The main breakthrough in the study came when the research team carefully timed the addition of growth factors to the iPSCs. Previous research showed the ability for iPSCs to be transformed into a common type of cell found in the skin called keratinocytes. By timing the addition of the growth factors, they were able to turn over 25% of the iPSCs into epithelial stem cells in a little more than two weeks. This “mass production” of epithelial stem cells holds tremendous promise for the development of a hair regeneration treatment. On this development, Dr. Xu said, “This is the first time anyone has made scalable amounts of epithelial stem cells that are capable of generating the epithelial component of hair follicles.”

As noted in a University of Pennsylvania press release on the news, there are two types of stem cell that are critical in hair follicles: epithelial stem cells and dermal papillae. While this study only achieved success in the creation of epithelial stem cells, we have extensively covered Dr. Angela Christiano’s ground-breaking research into the induction of dermal papillae into hair follicles (a process she calls hair follicle neogenesis).

“When a person loses hair, they lose both types of cells. We have solved one major problem, the epithelial component of the hair follicle. We need to figure out a way to also make new dermal papillae cells, and no one has figured that part out yet,” said Dr. Xu.

Once that it is done, we must also find a way to have the epithelial and dermal components of the follicle interact before one will be able to produce cosmetically useful hair. But with each successive breakthrough, the time when a scientist can use hair cloning techniques to regenerate human hair, and the surgeon can implant them into a person’s scalp, draws ever closer.

Reference
Yang R, Zheng Y, Xu X. Generation of folliculogenic human epithelial stem cells from induced pluripotent stem cells. Nature Communications. 2014.

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Q: I read, with considerable interest, your excellent article on the latest in Dr. Angela Christiano’s work on follicular neogenesis. It seems to me that the next questions we should be asking are: when will testing begin on human subjects and when might her research develop into a hair cloning treatment that is available to the general public?

A: It is very difficult to determine when this phase of the research might begin and it is even harder to predict when treatment might become available. First, the technology is not quite there. Dr. Christiano showed in her recent paper that changing the environment of skin (fibroblast) cells so that they could form into 3-D cultures enabled them to induce human hair-follicle growth. Although this was a major step towards cloning hair, additional work needs to be done before we will be able to mass produce fully-functioning human hair follicles to the extent needed for hair transplantation.

In addition, research on human subjects requires that experiments meet rigorous federal regulatory standards and these take time to be approved and carried out. Supposing that further study of follicle neogenesis results in a breakthrough treatment for hair loss, this treatment would still require meeting substantial efficacy and safety requirements of the FDA before it would be made available to the public. We will be communicating important developments as they occur through our Hair Cloning Research section and through periodic updates in the Bernstein Medical Newsletter.

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For four decades, scientists have known about the possibility of using cells derived from the base of hair follicles (dermal papilla cells) to stimulate the growth of new hair. More recently, researchers have been able to harvest dermal papillae, multiply them, and induce the creation of new hair follicles – but only in rats. Now, for the first time, scientists at Columbia University have shown in a new study that they can induce new human hair growth from cloned human papillae. This procedure, called “hair follicle neogenesis,” has the potential to solve one of the primary limitations in today’s surgical hair restoration techniques; namely, the patient’s finite donor hair supply that is available for transplantation.

A significant number of hair loss patients do not have enough donor hair to be candidates for a hair transplant procedure with the percentage of women lacking stable donor hair greater than in men. This technique would enable both men and women with limited donor reserves to benefit from hair transplant procedures and enable current candidates to achieve even better results.

According to co-study leader Angela M. Christiano, Ph.D., of Columbia University in New York, the ground-breaking publication is a “substantial step forward” in hair follicle neogenesis. While the technology still needs further development to be clinically useful, the implications of successfully inducing new hair follicles to grow from cloned hair cells could be a game-changer in the arena of hair restoration. Instead of moving hair follicles from the donor area to the recipient area, as in a hair transplant, follicular neogenesis involves the creation of new follicles, literally adding more follicles to the scalp rather than merely transplanting them from one part of the scalp to another. Regarding the new technique’s possible use as a hair restoration treatment, Dr. Christiano said:

“This method offers the possibility of inducing large numbers of hair follicles or rejuvenating existing hair follicles, starting with cells grown from just a few hundred donor hairs. It could make hair transplantation available to individuals with a limited number of follicles, including those with female-pattern hair loss, scarring alopecia, and hair loss due to burns.”

In hair follicle neogenesis, the physician would harvest a sample of healthy, hair-producing scalp tissue from a patient. The dermal papilla cells in the samples would be isolated and allowed to multiply in a laboratory culture, and then the lab-grown papillae would be injected back into balding areas of the person’s scalp where they would induce skin cells to form into hair follicles that would grow normal adult hairs.

The main hurdle that researchers had to overcome was getting human papillae to aggregate — or clump together — so that it could then develop into a follicle. Cells that are cultured on a flat surface seem to lose their ability to produce hair. Prior studies have shown that rat papillae, unlike human papillae, tend to aggregate spontaneously; a process that makes the next, critical step of forming the hair follicle possible. The research team reasoned that if they could create an extracellular environment in which human cells could aggregate, they could induce the growth of human hair follicles.

The breakthrough came as a result of encouraging human dermal papillae cells to grow in a three-dimensional culture — a spherical mass of cells — rather than in a conventional two-dimensional tissue culture. The 3-D configuration allows the cells to signal one another and direct the formation of a new hair. Normally, a culture is grown in a one-cell layer in a petri dish, however, in order to coax the papillae to aggregate, the researchers used a technique called a “hanging drop culture.” Here, droplets of culture, each containing the requisite number of papilla cells (about 3,000 cells) to form a hair follicle, are placed on the lid of a petri dish. When the lid is flipped upside-down, the force of gravity pulls the papillae into the bottom of the suspended droplet, causing the cells to ‘clump.’ This is similar to what the rat papillae do naturally.

In the study, Christiano and colleagues took dermal papillae from seven donors and cloned the cells in tissue culture. After a few days, the cells were transplanted into human skin that had been grafted onto the backs of mice. In implanting these cultured ‘clumps’ of dermal papillae, the research team induced hair follicle production in five out of seven test samples. Using a technique called gene expression analysis, the researchers were able to determine that the three-dimensional cultures restored 22% of the gene expression found in normal hair follicles, enough to induce the formation of new hairs that genetically matched the human donor’s DNA (rather than the mouse).

While hair cloning and multiplication techniques have been discussed and studied for years, the progress made by Dr. Christiano and her colleagues Colin Jahoda, Ph.D., and Claire Higgins, Ph.D. (the first author on the study), is unprecedented. In identifying the key benefit their procedure might have over current hair restoration practices, Dr. Christiano said:

“Current hair-loss medications tend to slow the loss of hair follicles or potentially stimulate the growth of existing hairs, but they do not create new hair follicles. Neither do conventional hair transplants, which relocate a set number of hairs from the back of the scalp to the front. Our method, in contrast, has the potential to actually grow new follicles using a patient’s own cells.”

In addition to combating male and female pattern genetic hair loss (androgenetic alopecia), the technique has the potential for use as a treatment for patients with severe skin injuries, such as burn victims, or sufferers of chronic conditions like scarring alopecias. In these cases, the absence of hair follicles had limited the usefulness of transplanted skin. With the ability to clone follicles, this problem can potentially be overcome.

Dr. Christiano, a colleague of Dr. Bernstein’s at Columbia University, is a world-renowned hair geneticist and a sufferer of alopecia areata, an autoimmune disease that creates bald spots on the scalp. In investigating the causes of her own balding, Dr. Christiano embarked on a career that led to she and her team identifying multiple genes associated with the disease. Her co-study leader, Dr. Jahoda, is a professor of stem cell sciences at Durham University and co-director of the North East England Stem Cell Institute. The lead author of the study, Dr. Higgins, is an associate research scientist in the dermatology department at Columbia University.

The study called, “Microenvironmental reprogramming by three-dimensional culture enables dermal papilla cells to induce de novo human hair-follicle growth,” and published in the Proceedings of the National Academy of Sciences (PNAS). The human hair follicles in this study were donated by volunteer hair transplant patients at Bernstein Medical – Center for Hair Restoration in New York City. We are appreciative of our patients who participated in this research.

Reference
Higgins, C.A., Chen, J.C., Cerise, J.E., Jahoda, C.A., Christiano, A.M.: Microenvironmental reprogramming by three-dimensional culture enables dermal papilla cells to induce de novo human hair-follicle growth. PNAS, 2013; doi: 10.1073/pnas.1309970110.

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We have previously discussed Dr. Angela Christiano‘s work on hair loss genetics with her team at Columbia University in New York. A review of the 16th annual meeting of the European Hair Research Society; held recently in Barcelona, Spain; brings to our attention new research being conducted by a very astute scientist, Dr. Claire Higgins, who works at Dr. Christiano’s laboratory.

With tissue supplied by Bernstein Medical, Dr. Higgins is studying the inductive properties of the dermal papilla (DP), a group of cells that forms the structure directly below each hair follicle. As outlined in our Hair Cloning Methods page, the dermal papilla is of great interest to hair restoration physicians. Ideally, research of this kind will lead to a breakthrough in hair cloning or hair multiplication which will allow physicians to effectively “cure” hair loss by developing a limitless supply of donor hair that can be used in hair restoration procedures.

A description of Dr. Higgins’ work is provided by the Hair Transplant Forum International:

“After isolating [dermal papilla] from human hair follicles, they grow the human DP cells in spheroid cultures in order to retain their inductive potential. Then they place the dermal papilla spheres between the epidermis and dermis of neonatal foreskin and graft it onto the back of mice. Human [hair follicle] neogenesis can be observed after 6 weeks.”

In essence, the scientists were able to capitalize on the potential of dermal papilla cells to induce the growth of a hair follicle by enclosing the DP cells in a small sphere. When implanted, the DP cells maintained their properties of inducing the development of follicles, and, indeed, follicles did grow.

It is another example of how far our understanding of the biology of hair has come in the last 10 years. And it is another example of scientists closing in on the elusive “hair loss cure.”

Read up on the latest Hair Cloning Research

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Q: There was a retrospective study by Lotufo et al. linking male pattern baldness to heart disease. Do you think there are other links like this for androgenetic alopecia? — J.L., San Francisco, CA

A: Family studies revealed both the androgen receptor locus on the X chromosome, as well as a new locus on chromosome 3q26. Association studies performed in two independent groups revealed a locus on chromosome 20 (not near any known genes) as well as the androgen receptor on the X chromosome.

So far, the genetic studies for androgenetic alopecia (AGA) have not revealed identification of a particular gene other than the androgen receptor, as well as the two candidate regions on chromosomes 3 and 20. Inasmuch as the androgen receptor can be involved in other diseases, this might be a feasible connection. Until candidate genes are identified that underlie AGA, it is impossible to predict where the commonalities might lie.

Excerpted from Angela Christiano, Hair Transplant Forum International 2011; 21(1): 14-15.

Read more about Hair Loss Genetics, and see some other Hair Restoration Answers posts on the topic.

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Dr. Christiano Interviewed on Alopecia, Hair Loss by New York TimesDr. Angela Christiano, a colleague of Dr. Bernstein’s at Columbia University, has been studying the causes of alopecia areata and genetic hair loss for many years. She, in fact, suffers from the disease as well.

The New York Times has published a question and answer interview with Dr. Christiano which covers her own struggle with alopecia, her research into the causes of genetic hair loss, and where she sees the field going in the future. Here is one exchange that offers a window into how her research is breaking new ground in the field of hair loss genetics:

Q. When were you able to actually do the study?

A. In 2008. We published our findings this past July. Ours was the first study of alopecia to use a genome-wide approach. By checking the DNA of 1,000 alopecia patients against a control group of 1,000 without it, we identified 139 markers for the disease across the genome.

We also found a big surprise. For years, people thought that alopecia was probably the stepchild of autoimmune skin diseases like psoriasis and vitiligo. The astonishing news is that it shares virtually no genes with those. It’s actually linked to rheumatoid arthritis, diabetes 1 and celiac disease.

Continued discovery by Dr. Christiano and others in the field of hair loss genetics will lead to clues like these, which will shape the future of hair loss treatment. The hope for hair loss sufferers around the world is that a medical treatment can be developed which will effectively cure androgenetic alopecia, or common baldness. There is a lot of ground to be covered and there are many studies yet to be conducted, but progress is being made.

You can read more about Dr. Christiano’s research on our Hair Loss Genetics News page.

Read the article and listen to a two minute audio stream of the interview at the NYT.

Photo c/o Ruth Fremson/The New York Times

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Dr. Angela Christiano of Columbia University in New York and a team of scientific researchers have identified a new gene involved in hair growth. Their discovery may affect the direction of future research for hair loss and the diagnosis and ultimate prevention of male pattern baldness.

The condition which leads to thinning hair is called hereditary hypotrichosis simplex. Through the study of families in Pakistan and Italy who suffer from this condition, the team was able to identify a mutation of the APCDD1 gene located in chromosome 18. This chromosome has been linked to other causes of hair loss.

According to Dr. Christiano, “The identification of this gene underlying hereditary hypotrichosis simplex has afforded us an opportunity to gain insight into the process of hair follicle miniaturization, which is most commonly observed in male pattern hair loss or androgenetic alopecia.”

The mutation of the APCDD1 gene inhibits the Wnt signaling pathway. Although this recently discovered gene does not explain the complex process of male pattern baldness, the importance of this discovery lies in the Wnt signaling that the gene directs, has now been shown to control hair growth in humans, as well as in mice.

Reference: Nature 464, 1043-1047 (15 April 2010) | doi:10.1038/nature08875;

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