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MICROBIOLOGY/GENETICS

Two New Mutations Found to Cause Baldness

- Hypotrichosis simplex and woolly hair

By: Stefan Anitei, Science Editor

Our scalp has about 100,000 hair follicles. About 100 of them stop working daily and, consequently, hairs fall. But at the same rate they are replaced. Of course, this is the case when baldness is not encoded in your genes.

Scientists are still trying to understand the pathway
of baldness genetics, but two recent researches come to explain a little bit more. It appears that each type of baldness is caused by specific genes...

A team lead by geneticist Regina Betz, from the University of Bonn, has discovered a gene (P2RY5) that triggers a rare type of hair loss named Hypotrichosis simplex. This is the result of a 6-year study made among families in Saudi Arabia. The study published in 'Nature Genetics' points that this is the first receptor protein found to be involved in hair growth.

"Although Hypotrichosis simplex is very uncommon, it may prove critical in our search for an understanding of the mechanisms of hair growth," said Betz.

This type of hair loss affects both men and women, even from childhood, not being testosterone-connected. The mutation of this gene impedes the normal formation of the P2RY5 receptors on the surface of hair follicle cells. These receptors are important for the binding of messengers that trigger the normal functioning of the hair cell.

"We can now search selectively for related substances that may be used in therapies for very different types of hair loss," said Ivar von Kügelgen from Bonn's Institute of Pharmacology and Toxicology.

Another team led by Angela Christiano of Columbia University discovered another mutation of the same gene that causes the "woolly hair" (sparse, dry and tightly curled scalp hair). The research was made examining Pakistani families, and the mutation was found to affect the inner root sheath of hair follicles, which fix and shape individual hairs.

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26th February 2008, 07:40 GMT | Copyright (c) 2008 Softpedia | Contact:
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