Age-related hearing loss (ARHL), or presbycusis, is a complex auditory disorder that impairs spectral, temporal and spatial auditory perceptions in the aged. One of the more common deficits is a shift in the audiometric thresholds, which is most likely to be manifested peripherally due to pathological changes in the cochlea. It has been hypothesized that different patterns of ARHL emerge in the human as the result of distinct cochlear pathologies 
, although this dataset is necessarily limited. Subsequent studies in humans have indicated that while there are examples where a single cochlear pathology can account for changes in audiometric thresholds, there are approximately 25% of cases that result from mixed cochlear pathologies 
, and in most cases there are complex interactions between different elements of the cochlea (e.g. see 
). This is similar to studies in rodents, where either single or multiple pathologies can exist depending on the strain (reviewed by 
How these rodent models can relate to human ARHL remains unclear, and how to relate the results from the different species relies heavily on the questions being addressed and the strain of animals being used. One advantage of broadening the animal models to non-human primates is that the ascending auditory nervous system, particularly the cerebral cortex, is more similar between humans and monkeys compared to humans and rodents, allowing for a better understanding of the cortical contributions to central processing deficits 
. Accumulating evidence from behavioral and electrophysiological studies suggests that rhesus monkeys also experience ARHL 
. Bennett et al. 
reported age-related changes in both their middle-aged and old groups of monkeys that were primarily due to high-frequency hearing loss. The auditory brainstem response has been used to assess auditory thresholds to clicks 
and high frequency tones 
in macaque monkeys. In their most recent study, Fowler et al., 
found that high-frequency hearing loss increases with age, and that hearing impairments at mid frequencies increased after 21 years of age. These combined results strongly suggest that rhesus monkeys experience at least one form of ARHL. To our knowledge, there has been only one publication on the age-related histopathological changes in the cochlea of the rhesus monkey, and the results from that study were inconclusive. Hawkins et al. 
showed a progressive loss of hair cells that extended from both the lower base and upper apex with increasing age. They also reported a decrease of spiral ganglion cells that appeared to be primarily restricted to the base of the cochlea, but this pattern was not quantified.
Recently, we have found age-related broadening of spatial tuning curves and impaired gap processing in auditory cortex in two aged rhesus monkeys 
. This suggests that the age-related histopathological changes in the cochlea of the rhesus monkey may be more extensive that what was previously reported by Hawkins et al 
. To test this hypothesis and to gain a better understanding of the potential origin of acoustic processing deficits, we directly related auditory brainstem response (ABR) thresholds to clicks and pure tones to the histopathological changes in the cochlea in order to investigate how aging influences audiometric changes in rhesus monkeys. We found that normal aging is strongly associated with decreasing ABR sensitivity and extensive changes across multiple cochlear histopathologies in rhesus monkeys.