Public Release: 

Mouse model gives insight to human hair loss

Blackwell Publishing Ltd.

A progressive skin disease causing hair loss in adult humans was identified in laboratory mice, providing a genetic tool to study the disease known as alopecia areata (AA).

"Our mouse model has proven to be very useful as a preclinical model to test new treatments for alopecia areata before being used in humans," states lead researcher, John P. Sundberg, D.V.M., Ph.D., of The Jackson Laboratory inBar Harbor, Maine. The study further provided the opportunity to use newly available gene array technology to study AA's molecular mechanisms.

In this 5-year study, published in the Journal of Investigative Dermatology, researchers identified a virtually identical mouse model for human adult onset AA and were able to reproduce the disease for exploring treatments. Data revealed that the disease has a complicated genetic basis that involves 4 or more genes. These genes include those involved in susceptibility to the disease and genes that regulate pigmentation of the skin and hair.

"This [study] provides data for analyzing the genetic candidates responsible for AA as well as insights into other conditions, such as thyroid disorders, which have been associated with AA subsets," as summarized in the November "Clinical Snippets" published in the journal. "Random genome-wide linkage screenings in mice and humans can lead to greater understanding of AA and other complex polygenic diseases."

Alopecia areata is a highly unpredictable, autoimmune skin disease resulting in the loss of hair on the scalp and elsewhere on the body, according to the National Alopecia Areata Foundation. The condition is common, affecting both males and females in approximately 1.7 percent of the world population overall. This accounts for more than 4.7 million people in the United States alone.


This study is published in the Journal of Investigative Dermatology. Media wishing to receive a PDF of this article please contact

About the Authors
Dr. John P. Sundberg is a veterinary anatomic pathologist who has focused on genetic based skin and hair diseases in mutant laboratory mice for almost 20 years. Kathleen A. Silva is the chief technician in his laboratory and was in charge of the breeding colony and genotyping. Dr. Renhua Li is a biostatistician specializing in complex polygenic trait analysis and was instrumental in analyzing the genotyping data. Dr. Gregory Cox is a molecular geneticist who helped analyze the data and work with Drs. Sundberg and Lloyd E. King to identify the important genes in the susceptibility intervals. Dr. King is an M.D. dermatopathologist who has played a key role in our research to help us do direct comparisons with human alopecia areata. It has taken a team approach to make discoveries using this complex model.

Dr. Sundberg can be reached for questions and interviews at For more information on related issues, contact The Jackson Laboratory Public Information Program at 207-288-6051 or

About the Journal of Investigative Dermatology
The Journal of Investigative Dermatology (JID) publishes papers describing original research relevant to all aspects of cutaneous biology and skin disease. The spectrum of interest is indicated by the breadth of the editorial staff and includes biochemistry, biophysics, carcinogenesis, cellular growth and regulation, clinical research, development, epidemiology, extracellular matrix, genetics, immunology, melanocyte biology, microbiology, molecular and cell biology, pathology, pharmacology and percutaneous absorption, photobiology, physiology, and structure. It is published on behalf of the Society for Investigative Dermatology (SID) and the European Society for Dermatological Research (ESDR).

About Blackwell Publishing
Blackwell Publishing is the world's leading society publisher. The company remains independent with over 900 staff members in offices in the US, UK, Australia, China, Denmark, Germany, and Japan. Blackwell publishes over 700 journals in partnership with more than 550 academic and professional societies.

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