From Our 2010 Archives
New Hair Loss Gene Is Identified
Genetic Mutation May Play Role in Male Pattern Baldness and a Rare Hair Loss Disorder
Reviewed By Laura J. Martin, MD
April 14, 2010 -- A gene responsible for a rare hair loss disorder may also play an important role in male pattern baldness, according to a new study.
Researchers have identified a genetic mutation involved in hypotrichosis simplex, a hereditary hair loss disorder that affects less than 200,000 Americans. The disorder causes hair follicle miniaturization, a process in which hair follicles shrink and narrow, and thick hair is replaced by fine, downy "peach fuzz" hair.
But researchers say that the same process is also a key component of male pattern baldness.
"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," says researcher Angela M. Christiano, PhD, professor of dermatology and genetics and development at Columbia University Medical Center, in a news release.
The study, published in Nature, highlights the role of a mutated version of the gene APCDD1 in hair follicle biology.
Previous research has already linked the gene to other hair loss disorders, but in this study researchers found the mutated gene inhibits a signaling pathway involved in hair growth.
By learning more about this pathway, known as the Wnt pathway, researchers say the discovery may lead to new and improved treatments for male pattern baldness and other hair loss disorders.
"We have at last made a connection between Wnt signaling and human hair disease that is highly significant," says Christiano. "And unlike commonly available treatments for hair loss that involve blocking hormonal pathways, treatments involving the Wnt pathway would be non-hormonal, which may enable many more people suffering from hair loss to receive such therapies."
SOURCES: Shimormura, Y. Nature, April 15, 2010; vol 464: pp 1043-1046.
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