Physiological and histological evaluations of the cochlea between 3xTg-AD mouse model of Alzheimer’s diseases and R6/2 mouse model of huntington’s diseases

Sheue Er Wang, Chung Hsin Wu

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Patients with Alzheimer’s diseases (AD) and Huntington’s diseases (HD) are known to have abnormal auditory processing, but the physiological and histological evaluations of the cochlea between AD and HD have not been thoroughly assessed. Thus we assessed the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE), and then examined spiral ganglion neurons (SGNs) and hair cells in the cochlea using 3xTg-AD mouse model of AD and R6/2-HD mouse model of HD. We found that the threshold of ABR, but not DPOAE, was significantly increased in AD mice from 9 months of age and thereafter. The significant loss of SGNs, but not hair cells, was observed in the cochlea of 9- and 12-month AD mice. On the other hand, we found that both ABR and DPOAE thresholds were significantly increased in HD mice from 2 months of age and thereafter. The large loss of hair cells and the small loss of SGNs were observed in the cochlea of 3-month HD mice. Furthermore, the prestin expression in outer hair cells (OHCs) was significantly decreased in HD mice from 2 months of age and thereafter, and the loss of prestin expression was earlier before OHCs death in HD mice. Different from HD mice, the prestin expression in OHCs in AD mice was not changed even at 12 months of age. Our data suggest that cochlear pathology contributing to hearing loss is quite different between transgenic mice of AD and HD. More detailed pathological mechanisms for hearing loss between AD and HD need further study.

Original languageEnglish
Pages (from-to)359-366
Number of pages8
JournalChinese Journal of Physiology
Volume58
Issue number6
DOIs
Publication statusPublished - 2015 Jan 1

Fingerprint

Cochlea
Huntington Disease
Alzheimer Disease
Outer Auditory Hair Cells
Spiral Ganglion
Brain Stem Auditory Evoked Potentials
Hearing Loss
Neurons
Alzheimer disease type 2
Alopecia
Transgenic Mice
Cell Death
Pathology

Keywords

  • Alzheimer’s disease
  • Auditory brainstem response
  • Cochlear pathology
  • Distortion product otoacoustic emissions
  • Hearing loss
  • Huntington’s disease
  • Prestin
  • Transgenic mice

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Physiological and histological evaluations of the cochlea between 3xTg-AD mouse model of Alzheimer’s diseases and R6/2 mouse model of huntington’s diseases",
abstract = "Patients with Alzheimer’s diseases (AD) and Huntington’s diseases (HD) are known to have abnormal auditory processing, but the physiological and histological evaluations of the cochlea between AD and HD have not been thoroughly assessed. Thus we assessed the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE), and then examined spiral ganglion neurons (SGNs) and hair cells in the cochlea using 3xTg-AD mouse model of AD and R6/2-HD mouse model of HD. We found that the threshold of ABR, but not DPOAE, was significantly increased in AD mice from 9 months of age and thereafter. The significant loss of SGNs, but not hair cells, was observed in the cochlea of 9- and 12-month AD mice. On the other hand, we found that both ABR and DPOAE thresholds were significantly increased in HD mice from 2 months of age and thereafter. The large loss of hair cells and the small loss of SGNs were observed in the cochlea of 3-month HD mice. Furthermore, the prestin expression in outer hair cells (OHCs) was significantly decreased in HD mice from 2 months of age and thereafter, and the loss of prestin expression was earlier before OHCs death in HD mice. Different from HD mice, the prestin expression in OHCs in AD mice was not changed even at 12 months of age. Our data suggest that cochlear pathology contributing to hearing loss is quite different between transgenic mice of AD and HD. More detailed pathological mechanisms for hearing loss between AD and HD need further study.",
keywords = "Alzheimer’s disease, Auditory brainstem response, Cochlear pathology, Distortion product otoacoustic emissions, Hearing loss, Huntington’s disease, Prestin, Transgenic mice",
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AU - Wu, Chung Hsin

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N2 - Patients with Alzheimer’s diseases (AD) and Huntington’s diseases (HD) are known to have abnormal auditory processing, but the physiological and histological evaluations of the cochlea between AD and HD have not been thoroughly assessed. Thus we assessed the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE), and then examined spiral ganglion neurons (SGNs) and hair cells in the cochlea using 3xTg-AD mouse model of AD and R6/2-HD mouse model of HD. We found that the threshold of ABR, but not DPOAE, was significantly increased in AD mice from 9 months of age and thereafter. The significant loss of SGNs, but not hair cells, was observed in the cochlea of 9- and 12-month AD mice. On the other hand, we found that both ABR and DPOAE thresholds were significantly increased in HD mice from 2 months of age and thereafter. The large loss of hair cells and the small loss of SGNs were observed in the cochlea of 3-month HD mice. Furthermore, the prestin expression in outer hair cells (OHCs) was significantly decreased in HD mice from 2 months of age and thereafter, and the loss of prestin expression was earlier before OHCs death in HD mice. Different from HD mice, the prestin expression in OHCs in AD mice was not changed even at 12 months of age. Our data suggest that cochlear pathology contributing to hearing loss is quite different between transgenic mice of AD and HD. More detailed pathological mechanisms for hearing loss between AD and HD need further study.

AB - Patients with Alzheimer’s diseases (AD) and Huntington’s diseases (HD) are known to have abnormal auditory processing, but the physiological and histological evaluations of the cochlea between AD and HD have not been thoroughly assessed. Thus we assessed the auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE), and then examined spiral ganglion neurons (SGNs) and hair cells in the cochlea using 3xTg-AD mouse model of AD and R6/2-HD mouse model of HD. We found that the threshold of ABR, but not DPOAE, was significantly increased in AD mice from 9 months of age and thereafter. The significant loss of SGNs, but not hair cells, was observed in the cochlea of 9- and 12-month AD mice. On the other hand, we found that both ABR and DPOAE thresholds were significantly increased in HD mice from 2 months of age and thereafter. The large loss of hair cells and the small loss of SGNs were observed in the cochlea of 3-month HD mice. Furthermore, the prestin expression in outer hair cells (OHCs) was significantly decreased in HD mice from 2 months of age and thereafter, and the loss of prestin expression was earlier before OHCs death in HD mice. Different from HD mice, the prestin expression in OHCs in AD mice was not changed even at 12 months of age. Our data suggest that cochlear pathology contributing to hearing loss is quite different between transgenic mice of AD and HD. More detailed pathological mechanisms for hearing loss between AD and HD need further study.

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