ABSTRACT
Aside from investigations that directly measure aging changes of the human central auditory system, as summarized comprehensively by Willott (1991a), a strong case can be made that the most productive animal model for understanding the neural bases of presbycusis — age-related hearing loss — is the mouse. Mice have afforded many advantages along these lines. Different strains of mice lose their hearing at different rates. For example, CBA strains (e.g., CBA/J, CBA/CaJ) have a slow, relatively flat, progressive hearing loss with a time frame similar to that of humans, if one corrects for the different absolute lifespans of mice and men. In contrast, the DBA/2J (DBA) and C57BL/6J (C57) mouse strains have very rapid, high-frequency hearing losses. Comparing neural changes with age in these different strains allows for determination of peripheral vs. central etiologies. For example, a 6-month-old C57 mouse has a young brain, but an “old” ear; whereas, a 2-year-old CBA mouse has both an old ear and old brain. Last, breakthroughs in molecular biology, including mapping of the human and mouse genomes, make the mouse especially relevant for utilization of genetically engineered mice and development of gene therapies that eventually may cure or prevent age-related sensory disorders.
