The Bar Harbor conference was basic hair biology oriented rather than being directed at finding treatments. There were reviews on gene expression and techniques for locating genes in disease, extensive reviews on hair follicle morphology and also comparison of hair follicles to nails and teeth as related skin structures.
The highlights included a well known genetic researcher talking about the hairless gene. This has been demonstrated not to be involved in Androgenetic Alopecia. The researcher’s team has been applying the hr mutant gene to normal mice as a gene therapy. The application inhibited hair growth. Although at the (very) experimental stage, the researcher suggested it might be a possible gene therapy to treat excess hair growth. They have now identified several different forms of hairless gene mutation in humans, and several individuals previously diagnosed as having Alopecia Areata were found to have a hairless gene mutation after testing (congential or papular atrichia).
Dr Elise Olsen gave a review of Androgenetic hair loss in women and suggested that the ludwig grading system was not a good categorization method for female pattern baldness. She suggested a more complex categorization system based on hair parting width and the amount of hair loss in the frontal vertex region. This system is to be published shortly (Dr Olsen’s talk did not go down well with many of those attending, most of them are aware the Ludwig system is too simplistic).
Of special interest was an announcement during the conference that a grant application to the NIH to set up a central DNA repository for Alopecia Areata research had been awarded. The details have yet to be released but a central repository will help AA gene research considerably.
Genes and gene therapy was a big focus at the conference. Several seminars discussed gene expression during the hair cycle and showed that several wnt genes and the Noggin gene are fundamentally involved in hair cycling and growth. Gene therapy reviewed by Lorne Taichman showed that in principle it is possible to transfect hair follicle cells with genes and have gene expression persist for at least 16 weeks. His team transfected a lacZ reporter gene into mouse hair follicles and the gene activity was still present, albeit in a patchy manner, 16 weeks later. They are confident they had transfected hair follicle stem cells given the expression lasted so long.
Maybe of most interest to everyone was the talk by a representative from Merck. He gave the typical review of Finasteride but a few slides he flashed up were new. The most recent results on Propecia show that the individuals who have been using for 5 years now are starting to have a decline in hair density. Before the hair density had always gradually climbed year on year and the placebo users had progressively declined. However, both groups at year 5 had a drop in hair density although the propecia users still have much more hair than the placebo users.
The typical anagen growth phase for scalp hair lasts 4-5 years. So it was suggested that the decline was because the hair follicles, under the control of propecia, were entering a telogen phase at about the same time. Hair follicles cycle in a random mosaic pattern in humans but the cycle can be coordinated under the control of drugs like minoxidil and propecia. Merck may be hoping the hair density will bounce up again with next years results.
Merck very briefly discussed new treatments from themselves and Glaxo. Merck suggested there might be some dangers in using a type I and II 5 aplha reductase inhibitor such as Glaxo’s “Dutasteride” and “Turosteride” drugs. The 5 alpha reductase inhibitors would lead to a significant increase in testosterone and this could be transformed into estrogens by other enzymes in the body. Consequently, Merck suggested that there could be a risk of estrogen disorders in Dutasteride users.
He also briefly flashed up a slide on alternative drugs for AGA called “melformin” and “thiazolidinediones”.
All in all it was an extremely informative conference.