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NIDCD Director James Battey's 2014 Testimony to the Senate Subcommittee on Labor-HHS-Education Appropriations
DEPARTMENT OF HEALTH AND HUMAN SERVICES
NATIONAL INSTITUTES OF HEALTH
Fiscal Year 2014 Budget Request
Statement for the Record
Senate Subcommittee on Labor-HHS-Education Appropriations
James F. Battey, Jr., M.D., PhD.
Director, National Institute on Deafness and Other Communication Disorders
May 15, 2013
On this page:
- Researchers Restore Hearing in Noise-Deafened Mice
- Novel Approaches of Inner Ear Regenerative Therapies
- Researchers Identify Gene Linked to Progressive Hearing Loss from Noise and Aging
- NIDCD Supports Research to Develop a Vaccine Against an Emerging Type of Childhood Ear Infection
Mr. Chairman and Members of the Subcommittee:
I am pleased to present the President’s Budget request for the National Institute on Deafness and Other Communication Disorders (NIDCD) of the National Institutes of Health (NIH). The fiscal year (FY) 2014 NIDCD budget of $422,936,000 includes an increase of $7,436,000 over the comparable FY 2012 appropriation of $415,500,000.
NIDCD conducts and supports research, and research training in the normal and disordered processes of hearing, balance, smell, taste, voice, speech, and language. Our Institute focuses on disorders that affect the quality of life of millions of Americans in their homes, workplaces, and communities. The physical, emotional, and economic impact for individuals living with these disorders is tremendous. NIDCD continues to make investments to improve our understanding of the underlying causes of communication disorders, as well as their treatment and prevention. It is a time of extraordinary promise, and I am excited to be able to share with you some of NIDCD’s ongoing research and planned activities on communication disorders.
Researchers Restore Hearing in Noise-Deafened Mice
Our ability to hear relies on sensory hair cells in the inner ear. The hairs on these specialized cells convert sound vibrations into electrical signals, which travel to the brain by way of the auditory nerve. When hair cells are damaged—by disease, injury, or aging—a person experiences hearing loss, and mammals cannot regenerate these lost hair cells.
Researchers supported by NIDCD have shown for the first time that a drug can be used to grow sensory hair cells in the inner ear. They injected a drug into the cochlea (a spiral shaped organ in the inner ear that shelters hair cells) of mice made deaf by exposure to loud noise. The drug blocked a cell-signaling system known to keep stem cells in the inner ear from turning into hair cells. By blocking that particular pathway, the drug encouraged cells supporting and surrounding the hair cells to turn into new hair cells, which led to a small improvement in the mice’s hearing.
This is the first study to show that scientists can use a drug to restore partial hearing in a mouse with noise-induced hearing loss. Scientists now hope to develop similar treatments to reverse hearing loss in humans, especially among the estimated 36 million adult Americans who report hearing loss.
Novel Approaches of Inner Ear Regenerative Therapies
Although research to determine ways to regenerate inner ear hair cells is under way, there remains a lack of potential treatments to restore lost mammalian hair cell function. Research is needed to identify and facilitate important molecular switches and regulators that initiate and sustain mammalian hair cell repair.
NIDCD places a high priority in research that focuses on regenerative medicine. For example, the Institute is planning a research initiative for FY 2014 with the goal of developing hair cell regeneration strategies. NIDCD held a workshop, in September 2011, to identify opportunities to induce regeneration in the inner ear. As a result of this workshop, NIDCD issued a Funding Opportunity Announcement to encourage innovative and novel approaches to inner ear regenerative therapies research. The ultimate goal of the research is to identify and “turn on” important molecular switches and regulators to enable mammals to regenerate and repair their own inner ear hair cells. This research may result in therapies that will provide hope of future treatments for those who have lost hearing due to aging, injury, or noise exposure, including military veterans returning from active duty.
Another purpose of the initiative is to attract and support NIH-defined basic and clinical early-stage investigators (ESIs) to the area of biological repair of mammalian inner ear hair cells. NIDCD is especially interested in ESIs who bring new, innovative approaches, and strategies from scientific fields minimally represented in the NIDCD portfolio, such as tissue fabrication, biomaterials, and regenerative medicine. By supporting ESIs from other scientific areas, this initiative will encourage diversified approaches and an increased number of investigators focused on regenerative therapies in the inner ear.
Researchers Identify Gene Linked to Progressive Hearing Loss from Noise and Aging
An international team of scientists funded by NIDCD has identified the first gene in humans and mouse models that is associated with both noise-induced and age-related hearing loss. The gene, P2X2, appears to be crucial for the preservation of life-long normal hearing and for protection from exposure to loud noise. P2X2 is associated with the human gene locus DFNA41, a form of hearing loss that typically begins early in life (around 12-20 years of age), and progresses with age. High-frequency tinnitus (high-pitched ringing in the ears) often accompanies hearing loss associated with DFNA41.
The research team discovered that the P2X2 gene mutation found in DFNA41 results in defects in sensory hair cells in the inner ear, which eventually lead to ongoing hearing loss. The study establishes, at the cellular and molecular levels, that the function of this ion channel, previously known to be involved in sensory signaling of pain, has a major impact on noise-induced and age-related hearing loss.
These findings demonstrate the importance of genetic approaches to uncover the underlying mechanisms that contribute to hearing loss, either as a result of age or chronic exposure to noise. Importantly, identifying the P2X2 mutation may provide scientists with a way to develop targeted treatments for progressing hearing loss in humans with DFNA41, and may be applicable to the treatment of noise-induced and age-related hearing loss in the broader population.
NIDCD Supports Research to Develop a Vaccine Against an Emerging Type of Childhood Ear Infection
Ear infections during childhood are of great concern to NIDCD, because they not only cause pain and suffering, but they also interfere with a child’s ability to hear properly during a critical period of language development. Since 2000, childhood vaccines have prevented many ear infections caused by two strains of bacteria–Haemophilus influenzae and pneumococcus. However, doctors are now seeing an increase in the number of ear infections caused by another strain of bacteria, called Moraxella catarrhalis (M. catarrhalis).
NIDCD-supported scientists are working to understand how this bacterium infects humans and avoids destruction by the immune system. They hope to identify a particular structure (called an antigen) that is very similar among all strains of M. catarrhalis, so that a vaccine based on a single antigen will protect against as many strains of the bacterium as possible.
The research team is using bioinformatics to predict which M. catarrhalis proteins are likely to be found on the surface, to make an attractive antigen target. They are using gene chips to identify which genes are identical or similar among multiple strains of the bacterium, and then testing these in petri dishes and in animal models. The scientists are now testing several promising vaccine antigens against M. catarrhalis, and hope that a new vaccine could be ready for human testing in a few years.
James F. Battey, Jr., M.D., Ph.D.
Director, National Institute on Deafness and Other Communication Disorders
James F. Battey, Jr., received his Bachelor of Science degree in physics from the California Institute of Technology in 1974. He received an M.D. and Ph.D. in biophysics from Stanford University School of Medicine in 1980. After receiving training in pediatrics, he pursued a postdoctoral fellowship in genetics at Harvard Medical School under the mentorship of Dr. Philip Leder. Since completing his postdoctoral fellowship in 1983, he has held a variety of positions at the National Institutes of Health, serving in the National Cancer Institute, National Institute of Neurological Disorders and Stroke, and the National Institute on Deafness and Other Communication Disorders (NIDCD). Currently, he is the director of the NIDCD, and also serves as the vice chair of the NIH Stem Cell Task Force. He has been married for 30 years to Frances Battey, and has two sons, Michael and JJ.