Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss

2007 ◽  
Vol 226 (1-2) ◽  
pp. 185-193 ◽  
Author(s):  
Tatsuya Yamasoba ◽  
Shinichi Someya ◽  
Chikako Yamada ◽  
Richard Weindruch ◽  
Tomas A. Prolla ◽  
...  
2013 ◽  
Vol 51 (7-8) ◽  
pp. 588-602 ◽  
Author(s):  
Yu Ding ◽  
Jianhang Leng ◽  
Fan Fan ◽  
Bohou Xia ◽  
Pan Xu

Author(s):  
Juyong Chung

A number of studies have demonstrated a significant association between age-related hearing loss (ARHL) and cognitive decline. However their relationship is not clear. In this review, we focused on the etiological mechanisms between ARHL and cognitive decline to explain the nature of this relationship: 1) causal mechanisms (e.g., cognitive load hypothesis, cascade hypothesis); 2) common cause mechanisms (e.g., microvascular disease); 3) overdiagnosis or harbinger hypothesis. We conclude that no single mechanism is sufficient and hearing and cognition related to each other in several different ways. In addition, we reviewed the effectiveness of hearing intervention (e.g., hearing aids and cochlear implants) on cognition function, and the role of hearing aid use and cochlear implant depends on the relevant mechanism.


2018 ◽  
Vol 217 (10) ◽  
pp. 3327-3329 ◽  
Author(s):  
Laura E. Newman ◽  
Gerald S. Shadel

What causes inflammation in age-related neurodegenerative diseases remains a mystery. Sliter et al. (2018. Nature. https://doi.org/10.1038/s41586-018-0448-9) show that, when damaged mitochondria cannot be removed by mitophagy, stress from exercise or mitochondrial DNA mutations activates the proinflammatory cGAS–STING pathway that may contribute to Parkinson’s disease.


2010 ◽  
Vol 192 (1) ◽  
pp. 20-23 ◽  
Author(s):  
Julie M Schneider ◽  
Bamini Gopinath ◽  
Catherine M McMahon ◽  
Helena C Britt ◽  
Christopher M Harrison ◽  
...  

Antioxidants ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 109 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba

Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients.


2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Anna M. Czarnecka ◽  
Ewa Bartnik

Mitochondrial DNA mutations and polymorphisms have been the focus of intensive investigations for well over a decade in an attempt to understand how they affect fundamental processes such as cancer and aging. Initial interest in mutations occurring in mitochondrial DNA of cancer cells diminished when most were found to be the same mutations which occurred during the evolution of human mitochondrial haplogroups. However, increasingly correlations are being found between various mitochondrial haplogroups and susceptibility to cancer or diseases in some cases and successful aging in others.


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