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May 2003

Genetic Secrets of Baldness Slowly Receding


(HealthScoutNews)

Men and women with disappearing hairlines don't yet have reason to cheer, but the baldness puzzle may be a bit closer to a solution.

Scientists from Johns Hopkins University School of Medicine and CNRS-Institut Pasteur in France have developed a mouse model of inherited baldness.

They hope this genetically engineered model will further their current understanding -- which is sketchy -- of why some
humans go bald as they age but others maintain a healthy mane throughout life.

"I would not and could not say we've found the cause of human baldness," says Pierre Coulombe, a professor of biological chemistry and dermatology at Hopkins and lead author of the study appearing in tomorrow?s issue of Genes & Development. Rather, he is hopeful they have found something to build on in future research.

Hereditary hair loss is the most common form of hair loss and affects about 50 million men and 30 million women in the United States, according to estimates from the American Academy of Dermatology.

Coulombe's team engineered mice to lack the gene that encodes a specific keratin protein. Keratin proteins are found in the hair, nails and epidermis of people as well as in the fur, feathers, and hooves of animals. In all, there are nearly 30 keratin genes just in the hair
follicles, and Coulombe's team discovered that a defect in just one of them -- called keratin 17 (K17) -- could make mice go temporarily bald.

Mice in whom the K17 gene was removed did not grow fur within the first few weeks of their lives, as mice with the gene normally do. However, at about three weeks old, the mice with the removed K17 gene did begin to grow fur, Coulombe says.

The researchers found out that another keratin gene, K16, activated in response to the absence of the K17 gene. It took over, and compensated for the loss.

"In these mice lacking the K17 gene, the hair is not growing normally for two reasons," Coulombe says. "The hair may be fragile. And a subset of hair cells is committing suicide -- it's pre-programmed cell death."

Humans with defects in K17 have problems with their nails, sebaceous glands -- glands that empty into a hair follicle and secrete sebum, which includes fat, keratin and cellular material -- and hair, Coulombe says.

Their nails grow abnormally thick. Their sebaceous glands are enlarged, and their skin has a bumpy appearance. Their hair is also twisted and breaks easily, he says.

This is not the first mouse model of baldness, Coulombe says, noting that other scientists have also developed models. "There's no such thing as one baldness model," he says. "There are multiple reasons for baldness. Hair is such a complicated structure."

A hair loss expert familiar with the study praised it, but had a caveat. "This is an excellent study which increases our understanding of how an individual who may lack one gene necessary for normal keratin production may compensate with another gene," says Dr. Richard A. Strick, a clinical professor of dermatology and medicine at the University of California, Los Angeles, School of Medicine.

"And it also furthers our understanding of the difference in expression of a genetic abnormality between individuals who have that defect. However, this study does not in and of itself explain any of the common types of hair loss in people. Nor does it provide an animal experimental model for any major type of alopecia [hair loss] in humans."

However, Coulombe says that is a matter of opinion. "Understanding how the baldness occurs in these mice might help us understand how it occurs in humans.

There is no human baldness condition to which this [mouse model] corresponds. [But] our group has identified a gene that plays an important role in the formation of hair at the late stage," he says.

The new model, he adds, is going to help explain how hair tissue is produced in the first place and how it oscillates between growth and rest phases. The model might serve as a generic model rather than a specific one, Coulombe says. In the meantime, he adds, "We'll take what we can get."