Disturbance in the protein landscape of cochlear perilymph in an Alzheimer's disease mouse model

PLoS One. 2024 May 10;19(5):e0303375. doi: 10.1371/journal.pone.0303375. eCollection 2024.

Abstract

Hearing loss is a pivotal risk factor for dementia. It has recently emerged that a disruption in the intercommunication between the cochlea and brain is a key process in the initiation and progression of this disease. However, whether the cochlear properties can be influenced by pathological signals associated with dementia remains unclear. In this study, using a mouse model of Alzheimer's disease (AD), we investigated the impacts of the AD-like amyloid β (Aβ) pathology in the brain on the cochlea. Despite little detectable change in the age-related shift of the hearing threshold, we observed quantitative and qualitative alterations in the protein profile in perilymph, an extracellular fluid that fills the path of sound waves in the cochlea. Our findings highlight the potential contribution of Aβ pathology in the brain to the disturbance of cochlear homeostasis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Cochlea* / metabolism
  • Cochlea* / pathology
  • Disease Models, Animal*
  • Hearing Loss / metabolism
  • Hearing Loss / pathology
  • Mice
  • Mice, Transgenic
  • Perilymph* / metabolism

Substances

  • Amyloid beta-Peptides

Grants and funding

This work was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology (KAKENHI: 21K06421, 23H04167), Inamori Foundation, Brain Science Foundation, Narishige Fund, and Takeda Science Foundation to D.I.; AMED-CREST (23gm1510004) and Moonshot R&D (JPMJMS2024) to H.H. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.