{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:02:14Z","timestamp":1791183734714,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,9,23]],"date-time":"2004-09-23T00:00:00Z","timestamp":1095897600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Comparative Neurology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The predominant conceptual framework for understanding human age\u2010related hearing loss (ARHL, or presbycusis) holds that three different cochlear elements (organ of Corti, afferent neurons, and stria vascularis) can degenerate independently, and exert independent influences on hearing. Within this framework, temporal bones from subjects with ARHL may be classified as exemplifying <jats:italic>sensory<\/jats:italic> (referring to organ of Corti), \u201cprimary\u201d <jats:italic>neural<\/jats:italic> (loss of afferent neurons without loss of their hair cell targets), <jats:italic>strial<\/jats:italic>, or <jats:italic>mixed<\/jats:italic> ARHL. While there is general agreement as to the types of cochlear cells most affected by aging, there is less agreement about how to classify ARHL, and whether contributions of particular structures to hearing loss can be isolated. The cochlear apex of humans and animals is particularly prone to apparent primary loss of neurons that may represent an aspect of <jats:italic>neural<\/jats:italic> ARHL. We recently reported that in 129S6\/SvEv mice apical neuronal loss is often accompanied by abnormalities of spiral limbus, pillar cells, and Reissner's membrane (Ohlemiller and Gagnon [2004] J Comp Neurol 469:377\u2013390). We proposed that the initial pathology occurs within limbus, leading to disruption of perilymphatic ion homeostasis, and eventual loss of neurons as one consequence. We have now examined this issue quantitatively in young and old mice of four different strains (129S6\/SvEv, CBA\/J, C57BL\/6, and BALB\/c). Abnormalities of apical spiral limbus were found to correlate only weakly with neuronal loss. Strong correlations were found between neuronal loss and abnormalities of both pillar cells and Reissner's membrane, however. Apical neuronal loss and apical\u2010to\u2010basal progression of pathology of limbus, pillar cells, and Reissner's membrane run counter to most reported age\u2010related cochlear trends. Our findings suggest that these changes share a common triggering influence. J. Comp. Neurol. 479:103\u2013116, 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/cne.20326","type":"journal-article","created":{"date-parts":[[2004,9,23]],"date-time":"2004-09-23T21:00:30Z","timestamp":1095973230000},"page":"103-116","source":"Crossref","is-referenced-by-count":64,"title":["Apical\u2010to\u2010basal gradients in age\u2010related cochlear degeneration and their relationship to \u201cprimary\u201d loss of cochlear neurons"],"prefix":"10.1002","volume":"479","author":[{"given":"Kevin K.","family":"Ohlemiller","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia 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