Presbycusis, an age-related hearing loss, is accompanied by histopathologic
al cochlear changes including variable amounts of degeneration of the audit
ory receptors, neurons and the stria vascularis. The causes of degeneration
are unknown, although acoustic trauma and exposure to ototoxic agents are
certainly contributors to the cellular degeneration. Acquired mitochondrial
DNA defects are postulated as important determinants of aging in neuromusc
ular tissues. The cochlear neurons are highly metabolic and are, therefore,
likely to be affected by mitochondrial DNA defects. Sequence analysis has
demonstrated a significant number of acquired mutations in the cytochrome o
xidase gene in the neurons from aged human cochleas. The current study used
immunohistochemical labeling of cytochrome oxidase in the neuronal cell bo
dies in archival celloidin sections to evaluate relationships among label d
ensity, hearing loss, number of neurons and mitochondrial DNA changes withi
n individual cochleas. Label density was less in many aged temporal bones,
but not all. There was no relationship among any other variables. It is con
cluded that while there may be a decrease in the amount of cytochrome oxida
se expression in aged spiral ganglion cell bodies, there are many other fac
tors that contribute to hearing loss and cellular degeneration. (C) 2001 El
sevier Science B.V. All rights reserved.