Hearing loss related to aging (presbyacusis) is one of the major disorders affecting the elderly, yet we know very little about what causes the changes that occur in the auditory system and how these relate to hearing loss. Is human presbyacusis simply an aging of auditory structures, is it aging plus the summing of a lifetime of ototraumatic insults from noise, chemicals (drugs), and disease or are other factors such as changes in blood flow, increased free radical formation, genetically programmed neuronal cell death, increased susceptibility to noise or chemical damage or even diet significant? Is human presbyacusis not the result of """"""""pure aging"""""""" of auditory structures and this the reason no adequate animal model has been found? We have established a collaborative effort between the laboratories of anatomy, biochemistry and physiology of the Kresge Hearing Research Institute to elucidate mechanisms involved in the development of auditory sensory deficits in aging. We will perform morphological and neurochemical assessments in guinea pig and rat to test the following hypotheses: 1) That age-related loss of spiral ganglion cells and changes in inhibitory and excitatory circuitry in auditory brainstem and cochlea occur independently of changes in organ of Corti, 2) That there are age- related changes in cochlear blood flow, cochlear vessels and cochlear vascular reactivity, 3) That changes in the sensitivity of cochlear hair cells to ototraumatic insults occur with aging, 4) That free radical accumulation induces changes in lipid peroxidation, membrane lipid domains, membrane fluidity and function in aging, and 5) That increased fat and/or cholesterol diet influences the age-related changes listed above. Physiological assessments of auditory function will be performed for correlation with these parameters. This will provide us with information that will help us not only to better understand the origins and development of hearing loss in the elderly, but, to develop more effective methods of its treatment and prevention.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Project (R01)
Project #
5R01AG008885-04
Application #
3120683
Study Section
Sensory Disorders and Language Study Section (CMS)
Project Start
1990-03-01
Project End
1995-02-28
Budget Start
1993-03-01
Budget End
1994-02-28
Support Year
4
Fiscal Year
1993
Total Cost
Indirect Cost
Name
University of Michigan Ann Arbor
Department
Type
Schools of Medicine
DUNS #
791277940
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109
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Ren, T; Brown, N J; Zhang, M et al. (1995) A reversible ischemia model in gerbil cochlea. Hear Res 92:30-7
Brechtelsbauer, P B; Ren, T Y; Miller, J M et al. (1995) Autoregulation of cochlear blood flow in the hydropic guinea pig. Hear Res 89:130-6
Brown, J N; Miller, J M; Nuttall, A L (1995) Age-related changes in cochlear vascular conductance in mice. Hear Res 86:189-94
Miller, J M; Ren, T Y; Laurikainen, E et al. (1995) Hydrops-induced changes in cochlear blood flow. Ann Otol Rhinol Laryngol 104:476-83
Miller, J M; Ren, T Y; Nuttall, A L (1995) Studies of inner ear blood flow in animals and human beings. Otolaryngol Head Neck Surg 112:101-13
Nair, T S; Raphael, Y; Dolan, D F et al. (1995) Monoclonal antibody induced hearing loss. Hear Res 83:101-13
Ren, T; Nuttall, A L; Miller, J M (1995) Relative blood velocity measurement in individual microvessels using the self-mixing effect in a fiber-coupled helium-neon laser. Microvasc Res 49:233-45
Ren, T; Zhang, M; Nuttall, A L et al. (1995) Heart beat modulation of spontaneous otoacoustic emissions in guinea pig. Acta Otolaryngol 115:725-31

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