by : Karen Peralta
In the article: “Professor has discovered the genetic basis for hair loss” by John H. Tucker, Tucker talks about Angela Christiano a professor from the University of Columbia in New York city working at the dermatology and genetics development department. In 1996 Christiano was diagnosed with a disease called Alopecia Areata (AA). AA is a condition where hair falls out in patches. This condition affects 2% of the population about 5.3 million people in the U.S and the second most popular form of hair loss after male-pattern baldness. Chistiano decided to study hair loss due to her experience and minimal information there was about the genes that cause hair loss. Earlier this year she conducted a research study, where her team discovered that immune genes in AA are similar to some common diseases like celiac disease, diabetes type 1 and rheumatoid arthritis. This finding has given hope that drugs used to cure these diseases could be used for AA; in particular rheumatoid arthritis’ drugs.
AA works differently than male-pattern baldness because it has an unknown onset; patients loose hair not only from the head but other parts like their legs, eyebrows or eyelashes. AA is an autoimmune response disorder; this means that the immune system of the body has turned against the body, attacking organs in good condition. In this case the organ that is being attacked is hair throughout the body. Christiano’s team of researchers found a gene called ULBP3 through a genome wide association study (GWAS); a method that studies many SNPs (single nucleotide polymorphisms) to locate genes that causes a disease. The gene ULBP3 is turned off in normal hair follicles, but in AA ULBP3 is turned on. This is a bad sign because ULBP3 acts as a signaling light to immune killer cells. Immune killer cells carry a receptor called NKG2D which triggers an autoimmune response causing hair follicles to fall off. Even though Christiano’s team has started to find solutions, some of these are: blocking the NKG2D receptor using antibody drugs or using soluble receptors to block ULBP3 from being turned on. Besides AA, Christiano studies hypertrichosis (abnormal hair growth). According to Christiano, hair loss is one of many emotionally devastating diseases according to its quality of life index score. Recently she spoke at the AA foundation conference in Indianapolis; where she shared her experience and research. She also declared that these findings will open doors to find a solution for AA. More details can be found in her research paper published in Nature’s July 1st /10 issue.
This is a great article; it gives information about a disease that is not widely known and in need of funding. Christiano’s team not just informed us about AA, but showed us what they are doing to target it; by presenting the location, mechanism and solutions which many articles sometimes lack. This is a breakthrough in science; because this novel gene (ULBP3) not only opens doors to combat hair loss, but also to develop drugs or creams that induce hair loss for beauty purposes or people with hypertrichosis (excess hair). The fact that AA not only occurs in the head but other parts of the body would make women be first in line willing to pay for these types of treatments. Maybe knowing about both AA and hypertrichosis can complement each other in treatment by analyzing these diseases and tinkering with them until a solution is found. This article was interesting as it made me aware of something new. Plus, I like how it combines genetics with immunology which are two subjects I am currently studying.
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| Figure 1. Alopecia Areata (AA) patient. Source: Hair Center 2010. |
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| Figure 2. Many women struggle with hair removal products AA genes could help develop products to remove hair permanently. Source: The Fashionable house wife 2010. |
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| Figure 3 Hypertrichosis or Werewolf syndrome is the abnormal excess of hair growth disease, Studying AA could help people that suffer Hypertrichosis by perhaps activating genes responsible fo AA and vice versa. Source: www.xenophilius.wordpress.com 2010. |
