{"title":"耳鸣的耳蜗起源和作为耳鸣生物标志物的外毛细胞运动蛋白 Prestin","authors":"Erdoğan Bulut , Murat Arslan , Cem Uzun","doi":"10.1016/j.mehy.2024.111528","DOIUrl":null,"url":null,"abstract":"<div><div>Peripheral dysfunction and hearing loss are known risk factors for tinnitus; however, a portion of tinnitus patients exhibit no apparent peripheral auditory deficits. This article proposes that tinnitus may originate in the cochlea due to, undetectable damage to outer hair cells (OHCs) in individuals with normal hearing. The study further suggests that peripheral auditory deficits can be identified through the outer hair cell motor protein Prestin, which has potential as a biomarker for early detection. Minor OHC losses, which do not result in clinically detectable hearing loss, may lead to insufficient depolarization of inner hair cells (IHCs), thereby reducing sensory input along the cochlea-cortex pathway in the central auditory system. From a homeostatic gain control perspective, decreased amplification by OHCs, including abnormal electromotile responses, may lead to inadequate encoding by IHCs, contributing to the cochlear origin of tinnitus. Damage to OHCs that does not affect hearing thresholds, or abnormal electromotile contractions influenced by Prestin, may contribute to peripheral auditory dysfunction underlying tinnitus. As a result, pre-neural mismatched synchronization between OHCs and IHCs, driven by abnormal OHC electromotility, could cause sound processing disorders within the central auditory system. This pathophysiological mechanism at the cochlear level may lead to pathological alterations at multiple levels of the central auditory system. Prestin may serve as a potential biomarker for tinnitus, offering valuable insights into its cochlear origin and guiding future therapeutic developments.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"194 ","pages":"Article 111528"},"PeriodicalIF":2.1000,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cochlear origin of tinnitus and outer hair cell motor protein Prestin as a biomarker for tinnitus\",\"authors\":\"Erdoğan Bulut , Murat Arslan , Cem Uzun\",\"doi\":\"10.1016/j.mehy.2024.111528\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Peripheral dysfunction and hearing loss are known risk factors for tinnitus; however, a portion of tinnitus patients exhibit no apparent peripheral auditory deficits. This article proposes that tinnitus may originate in the cochlea due to, undetectable damage to outer hair cells (OHCs) in individuals with normal hearing. The study further suggests that peripheral auditory deficits can be identified through the outer hair cell motor protein Prestin, which has potential as a biomarker for early detection. Minor OHC losses, which do not result in clinically detectable hearing loss, may lead to insufficient depolarization of inner hair cells (IHCs), thereby reducing sensory input along the cochlea-cortex pathway in the central auditory system. From a homeostatic gain control perspective, decreased amplification by OHCs, including abnormal electromotile responses, may lead to inadequate encoding by IHCs, contributing to the cochlear origin of tinnitus. Damage to OHCs that does not affect hearing thresholds, or abnormal electromotile contractions influenced by Prestin, may contribute to peripheral auditory dysfunction underlying tinnitus. As a result, pre-neural mismatched synchronization between OHCs and IHCs, driven by abnormal OHC electromotility, could cause sound processing disorders within the central auditory system. This pathophysiological mechanism at the cochlear level may lead to pathological alterations at multiple levels of the central auditory system. Prestin may serve as a potential biomarker for tinnitus, offering valuable insights into its cochlear origin and guiding future therapeutic developments.</div></div>\",\"PeriodicalId\":18425,\"journal\":{\"name\":\"Medical hypotheses\",\"volume\":\"194 \",\"pages\":\"Article 111528\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2024-11-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical hypotheses\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0306987724002718\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical hypotheses","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306987724002718","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Cochlear origin of tinnitus and outer hair cell motor protein Prestin as a biomarker for tinnitus
Peripheral dysfunction and hearing loss are known risk factors for tinnitus; however, a portion of tinnitus patients exhibit no apparent peripheral auditory deficits. This article proposes that tinnitus may originate in the cochlea due to, undetectable damage to outer hair cells (OHCs) in individuals with normal hearing. The study further suggests that peripheral auditory deficits can be identified through the outer hair cell motor protein Prestin, which has potential as a biomarker for early detection. Minor OHC losses, which do not result in clinically detectable hearing loss, may lead to insufficient depolarization of inner hair cells (IHCs), thereby reducing sensory input along the cochlea-cortex pathway in the central auditory system. From a homeostatic gain control perspective, decreased amplification by OHCs, including abnormal electromotile responses, may lead to inadequate encoding by IHCs, contributing to the cochlear origin of tinnitus. Damage to OHCs that does not affect hearing thresholds, or abnormal electromotile contractions influenced by Prestin, may contribute to peripheral auditory dysfunction underlying tinnitus. As a result, pre-neural mismatched synchronization between OHCs and IHCs, driven by abnormal OHC electromotility, could cause sound processing disorders within the central auditory system. This pathophysiological mechanism at the cochlear level may lead to pathological alterations at multiple levels of the central auditory system. Prestin may serve as a potential biomarker for tinnitus, offering valuable insights into its cochlear origin and guiding future therapeutic developments.
期刊介绍:
Medical Hypotheses is a forum for ideas in medicine and related biomedical sciences. It will publish interesting and important theoretical papers that foster the diversity and debate upon which the scientific process thrives. The Aims and Scope of Medical Hypotheses are no different now from what was proposed by the founder of the journal, the late Dr David Horrobin. In his introduction to the first issue of the Journal, he asks ''what sorts of papers will be published in Medical Hypotheses? and goes on to answer ''Medical Hypotheses will publish papers which describe theories, ideas which have a great deal of observational support and some hypotheses where experimental support is yet fragmentary''. (Horrobin DF, 1975 Ideas in Biomedical Science: Reasons for the foundation of Medical Hypotheses. Medical Hypotheses Volume 1, Issue 1, January-February 1975, Pages 1-2.). Medical Hypotheses was therefore launched, and still exists today, to give novel, radical new ideas and speculations in medicine open-minded consideration, opening the field to radical hypotheses which would be rejected by most conventional journals. Papers in Medical Hypotheses take a standard scientific form in terms of style, structure and referencing. The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific communication, which ideas must eventually enter if they are to be critiqued and tested against observations.