Because hearing is accomplished by the brain (with neural input from the cochlea), presbyacusis can be ultimately accounted for by changes in brain activity that accompany aging. The anatomic and physiologic changes that accompany aging are of two basic types: the central effects of biological aging (CEBA) and the central effects of peripheral pathology (CEPP). Research using inbred mice and other animal models has provided insights into both CEPP and CEBA, and some implications of this research are reviewed, including the following. Age-related cochlear pathology results in changes in how frequency is "mapped" in the central auditory system (CAS), especially at higher anatomic levels, and this has potentially negative consequences for hearing. Aging and/or age-related hearing loss may impair neural inhibition in the CAS. CEPP may result in abnormalities in neural responses involved in binaural hearing and cause exaggerated "masking" of neural responses by noise. The extent of age-related anatomic change (CEBA and CEPP) varies among CAS subdivisions and accelerates during the terminal phase of life. Genes have been found to influence the time course and severity of presbyacusis as well as the role dietary restriction plays in ameliorating age-related hearing loss in mice.