Age-related auditory nerve deficits propagate central gain throughout the auditory system: Associations with cortical microstructure and speech recognition

IF 4 3区 医学 Q2 GERIATRICS & GERONTOLOGY
Neurobiology of Aging Pub Date : 2026-01-01 Epub Date: 2025-11-03 DOI:10.1016/j.neurobiolaging.2025.10.007
Emily M. Fabrizio-Stover , James W. Dias , Carolyn M. McClaskey , Kelly C. Harris
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Abstract

There is growing evidence that perceptual difficulties associated with age-related hearing loss are not solely due to cochlear damage and are exacerbated by central nervous system changes. We examined electrophysiological (EEG) responses to clicks and diffusion kurtosis imaging in 49 older (29 female) and 26 younger (20 female) adults to determine the extent to which auditory nerve (AN) deficits in older adults contributed to functional and structural changes throughout the auditory system. Older adults exhibited smaller AN responses, similar brainstem responses, and larger auditory cortex (AC) responses, demonstrating progressive “central gain.” Audiometric thresholds were not predictive of EEG measures. Reduced AN function predicted deficits in cortical microstructure (lower AC fractional anisotropy) in older adults, consistent with microstructure degeneration. These lower fractional anisotropy values in the AC of older adults also predicted larger AC responses and more central gain. Older adults exhibited significantly lower AC fractional anisotropy and kurtosis fractional anisotropy coupled with higher mean and radial diffusivity compared to younger adults. AC fractional anisotropy, radial diffusivity, axial diffusivity, and mean diffusivity were all significant predictors of speech-in-noise (SIN) recognition in older adults. The results suggest that reduced afferent input in older adults not only results in functional changes throughout the auditory system consistent with progressive gain but also contributes to deficits in AC structure beyond those explained by age alone, contributing to SIN recognition deficits. Understanding the complex effects of age, reduced AN input, central gain, and AC microstructure on SIN recognition may provide potential therapeutic targets for intervention.
与年龄相关的听神经缺损在整个听觉系统中传播中枢增益:与皮层微观结构和语音识别的关联。
越来越多的证据表明,与年龄相关的听力损失相关的感知困难不仅仅是由于耳蜗损伤,而且还会因中枢神经系统的变化而加剧。我们检测了49名老年人(29名女性)和26名年轻人(20名女性)对咔嚓声和弥散峰度成像的电生理(EEG)反应,以确定老年人听神经(AN)缺陷在多大程度上导致了整个听觉系统的功能和结构变化。老年人表现出较小的AN反应,类似的脑干反应和较大的听觉皮层(AC)反应,表现出进行性的“中枢增益”。听力阈值不能预测脑电图。AN功能降低预示着老年人皮层微结构缺陷(AC分数各向异性降低),与微结构退化相一致。老年人AC的低分数各向异性值也预示着更大的AC反应和更多的中心增益。与年轻人相比,老年人表现出明显较低的AC分数各向异性和峰度分数各向异性,同时具有较高的平均扩散系数和径向扩散系数。交流分数各向异性、径向扩散率、轴向扩散率和平均扩散率都是老年人语音噪声识别的显著预测因子。结果表明,老年人传入输入的减少不仅导致整个听觉系统的功能变化与进行性增益一致,而且还导致AC结构的缺陷,而不仅仅是年龄的原因,从而导致SIN识别缺陷。了解年龄、AN输入减少、中枢增益和AC微观结构对SIN识别的复杂影响可能为干预提供潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Neurobiology of Aging
Neurobiology of Aging 医学-老年医学
CiteScore
8.40
自引率
2.40%
发文量
225
审稿时长
67 days
期刊介绍: Neurobiology of Aging publishes the results of studies in behavior, biochemistry, cell biology, endocrinology, molecular biology, morphology, neurology, neuropathology, pharmacology, physiology and protein chemistry in which the primary emphasis involves mechanisms of nervous system changes with age or diseases associated with age. Reviews and primary research articles are included, occasionally accompanied by open peer commentary. Letters to the Editor and brief communications are also acceptable. Brief reports of highly time-sensitive material are usually treated as rapid communications in which case editorial review is completed within six weeks and publication scheduled for the next available issue.
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