scholarly journals Robust Neuronal Discrimination in Primary Auditory Cortex Despite Degradations of Spectro-temporal Acoustic Details: Comparison Between Guinea Pigs with Normal Hearing and Mild Age-Related Hearing Loss

2018 ◽  
Vol 19 (2) ◽  
pp. 163-180 ◽  
Author(s):  
Yonane Aushana ◽  
Samira Souffi ◽  
Jean-Marc Edeline ◽  
Christian Lorenzi ◽  
Chloé Huetz
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Guinea Pigs ◽  
Primary Auditory Cortex ◽  
Normal Hearing ◽  
Age Related ◽  
Age Related Hearing Loss

The miR-34a/Bcl-2 Pathway Contributes to Auditory Cortex Neuron Apoptosis in Age-Related Hearing Loss

2017 ◽  
Vol 22 (2) ◽  
pp. 96-103 ◽  
Author(s):  
Qiuhong Huang ◽  
Yongkang Ou ◽  
Hao Xiong ◽  
Haidi Yang ◽  
Zhigang Zhang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Molecular Mechanisms ◽  
Primary Auditory Cortex ◽  
Auditory Brainstem ◽  
Hearing Ability ◽  
Age Related ◽  
Brainstem Response ◽  
The Central Nervous System ◽  
Age Related Hearing Loss

Hypothesis: The miR-34a/Bcl-2 signaling pathway may play a role in the mechanisms related to age-related hearing loss (AHL) in the auditory cortex. Background: The auditory cortex plays a key role in the recognition and processing of complex sound. It is difficult to explain why patients with AHL have poor speech recognition, so increasing numbers of studies have focused on its central change. Although micro (mi)RNAs in the central nervous system have recently been increasingly reported to be associated with age-related diseases, the molecular mechanisms of AHL in the auditory cortex are not fully understood. Methods: The auditory brainstem response was used to assess the hearing ability of C57BL/6 mice, and q-PCR, immunohistochemistry, and Western blotting were used to detect the expression levels of miR-34a and Bcl-2 in the mouse auditory cortex. TUNEL and DNA fragmentation were adopted to detect the apoptosis of neurons in the auditory cortex. To verify the relationship of miR-34a and Bcl-2, we transfected an miR-34a mimic or miR-34a inhibitor into primary auditory cortex neurons. Results: In this study, miR-34a/Bcl-2 signaling was examined in auditory cortex neurons during aging. miR-34a and apoptosis increased in the auditory cortex neurons of C57BL/6 mice with aging, whereas an age-related decrease in Bcl-2 was determined. In the primary neurons of the auditory cortex, miR-34a overexpression inhibited Bcl-2, leading to an increase in apoptosis. Moreover, miR-34a knockdown increased Bcl-2 expression and diminished apoptosis. Conclusion: Our results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of AHL in the auditory cortex.

scholarly journals SUBCLINICAL AGE-RELATED HEARING LOSS IS INVERSELY ASSOCIATED WITH DEPRESSIVE SYMPTOMS

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S552-S552
Author(s):  
Justin S Golub ◽  
Katharine K Brewster ◽  
Adam Brickman ◽  
Adam Ciarleglio ◽  
José Luchsinger ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Depressive Symptoms ◽  
Pure Tone ◽  
Depression Scale ◽  
Pure Tone Audiometry ◽  
Normal Hearing ◽  
Health Study ◽  
Late Life Depression ◽  
Age Related ◽  
Age Related Hearing Loss

Abstract Age-related hearing loss (HL), defined by a pure-tone average (PTA) >25 decibels (dB) has been associated with depressive symptoms. We aimed to assess whether this association is present when hearing is better than the arbitrary, but widely-used, 25 dB threshold. The sampled population was the multicentered Hispanic Community Health Study (n=5,165). Cross-sectional data from 2008-2011 were available. Hearing was measured with pure tone audiometry. Clinically-significant depressive symptoms (CSDS) were defined by a score ≥10 on the 10-item Center for Epidemiologic Studies Depression Scale (CESD-10). Participants’ mean age was 58.3 years (SD=6.2, range=50-76). Among those with classically-defined normal hearing (PTA ≤25 dB), a 10 dB increase in HL was associated with 1.26 times the odds (95% CI=1.11, 1.42) of CSDS, adjusting for age, gender, education, vascular disease, and hearing aid use (p25 dB; p<0.001). Results held even for a stricter HL cutpoint of 15 dB. Among subjects with strictly normal hearing (PTA ≤15 dB), a 10 dB increase in HL was associated with 1.47 (1.14, 1.90) times the odds of CSDS, adjusting for confounders (p<0.01). Results also held when defining CSDS by an alternative CESD-10 score ≥16. In conclusion, increasing hearing thresholds were independently associated with CSDS among adults with subclinical HL (PTA ≤25 dB). Studies investigating whether treating HL can prevent late life depression should consider a lower threshold for defining HL.

Regulating Age-Related Hearing Loss with Bisphenol A via the Long Non-Coding RNA X Inactive Specific Transcript and MicroRNA-34a-5p Pathways

2020 ◽  
Vol 12 (8) ◽  
pp. 987-995
Author(s):  
Shifei Wang ◽  
Cheng Rao ◽  
Xingyu Huang ◽  
Tianhong Xie ◽  
Linling Su ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Bisphenol A ◽  
Auditory Cortex ◽  
Neuronal Cell ◽  
Specific Transcript ◽  
Age Related ◽  
Non Coding Rna ◽  
Lncrna Xist ◽  
Age Related Hearing Loss ◽  
Long Non Coding Rna

Age-related hearing loss (AHL) is a common, high-incidence, perceptual disease in the elderly population worldwide. Since bisphenol A (BPA) has been reported to associate with cell apoptosis, we hypothesize that BPA can inhibit the neuronal apoptosis in AHL. Forty Wistar rats were recruited to model AHL; they were then treated with different doses of BPA. We used auditory brainstem response testing to measure the BPA-induced improvement in the rats’ hearing. We examined the proliferation and apoptosis of the auditory cortical neurons in the rats with MTT assay and flow cytometry. Also, to delineate the underlying mechanism of BPA’s effect on AHL, we quantitated the expression level of long non-coding RNA X inactive specific transcript (lncRNA XIST) and miR-34a-5p in the rats’ auditory cortex with a novel method called nanoparticle PCR. We found that BPA intervention improved the hearing of AHL model rats, enhanced neuronal cell proliferation, restricted neuronal cell apoptosis, upregulated miR-34a-5p levels, and downregulated lncRNA XIST levels. The dual-luciferase reporter (DLR) assay revealed that BPA inhibited the apoptosis of auditory cortex neurons by targeting miR-34a-5p with lncRNA XIST and regulated the process of AHL. Therefore, we come to a conclusion that BPA contributes to the improvement of AHL, which may be achieved by upregulating miR-34a-5p and inhibiting the apoptosis of auditory cortex neurons via lncRNA XIST.

SIRT1 expression in the cochlea and auditory cortex of a mouse model of age-related hearing loss

2014 ◽  
Vol 51 ◽  
pp. 8-14 ◽  
Author(s):  
Hao Xiong ◽  
Min Dai ◽  
Yongkang Ou ◽  
Jiaqi Pang ◽  
Haidi Yang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Mouse Model ◽  
Auditory Cortex ◽  
Sirt1 Expression ◽  
Age Related ◽  
Age Related Hearing Loss

Expression of G9a in Auditory Cortex Is Downregulated in a Rat Model of Age-Related Hearing Loss

2020 ◽  
Author(s):  
Qian Li ◽  
Yang-hong Xiang ◽  
Xiao-jun Liang ◽  
Yun Zhang ◽  
Peng-peng Zhao ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Rat Model ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals Age-Related Hearing Loss Associations With Changes in Brain Morphology

2019 ◽  
Vol 23 ◽  
pp. 233121651985726 ◽  
Author(s):  
Mark A. Eckert ◽  
Kenneth I. Vaden ◽  
Judy R. Dubno
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
High Frequency ◽  
Latent Variables ◽  
Pure Tone ◽  
Brain Morphology ◽  
Medium Effect ◽  
Longitudinal Changes ◽  
Age Related ◽  
Age Related Hearing Loss

Age-related hearing loss has been associated with varied auditory cortex morphology in human neuroimaging studies. These findings have suggested that peripheral auditory system declines cause changes in brain morphology but could also be due to latent variables that affect the auditory periphery and brain. The current longitudinal study was designed to evaluate these explanations for pure-tone threshold and brain morphology associations. Thirty adults (mean age at Time 1 = 64.12 ± 10.32 years) were studied at two time points (average duration between visits = 2.62 ± 0.81 years). Small- to medium-effect size associations were observed between high-frequency pure-tone thresholds and auditory cortex gray matter volume at each time point. Although there were significant longitudinal changes in low- and high-frequency hearing measures and brain morphology, those longitudinal changes were not significantly correlated across participants. High-frequency hearing measures at Time 1 were significantly related to more lateral ventricle expansion, such that participants with higher measures exhibited larger increases in ventricle size. This ventricle effect was statistically independent of high-frequency hearing associations with auditory cortex morphology. Together, these results indicate that there are at least two mechanisms for associations between age-related hearing loss and brain morphology. Potential explanations for a direct hearing loss effect on brain morphology, as well as latent variables that likely affect both the inner ear and brain, are discussed.

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