Hearing Improvement in A/J Mice via the Mouse Nerve Growth Factor

Gao, Lixiang; Ge, Ruli; Xie, Gang; Yao, Dandan; Li, Ping; Wang, Oumei; Ma, Xiaoxue; Han, Fengchan

doi:10.21053/ceo.2016.01354

Cited by 9 publications

(6 citation statements)

References 23 publications

(30 reference statements)

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“…Several growth factors prevent degeneration of cochlear neurons, such as NGF [ 151 ], neurotrophic factor-3 (NT-3) [ 152 ], which have been shown to prevent ototoxic drug-induced hearing loss, NIHL and ARHL. However, some studies have found that the presence of hypertension and delayed treatment are negative factors related to the effectiveness of NGF treatment [ 153 ].…”

Section: Pathophysiological Mechanisms and Treatment Strategies Of Arhlmentioning

confidence: 99%

Age-related hearing loss and its potential drug candidates: a systematic review

Hu,

Sun,

et al. 2023

Chin Med

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Background Age-related hearing loss (ARHL) is one of the main illnesses afflicting the aged population and has a significant negative impact on society, economy, and health. However, there is presently no appropriate therapeutic treatment of ARHL due to the absence of comprehensive trials. Objectives The goal of this review is to systematically evaluate and analyze recent statistics on the pathologic classifications, risk factors, treatment strategies, and drug candidates of ARHL, including that from traditional Chinese medicine (TCM), to provide potential new approaches for preventing and treating ARHL. Methods Literature related to ARHL was conducted in databases such as PubMed, WOS, China National Knowledge Infrastructure (CNKI), and Wanfang from the establishment of the database to Jan, 2023. The pathology, causal factor, pathophysiological mechanism, treatment strategy, and the drug candidate of ARHL were extracted and pooled for synthesis. Results Many hypotheses about the etiology of ARHL are based on genetic and environmental elements. Most of the current research on the pathology of ARHL focuses on oxidative damage, mitochondrial dysfunction, inflammation, cochlear blood flow, ion homeostasis, etc. In TCM, herbs belonging to the kidney, lung, and liver meridians exhibit good hearing protection. Seven herbs belonging to the kidney meridian, 9 belonging to the lung meridian, and 4 belonging to the liver meridian were ultimately retrieved in this review, such as Polygonum multiflorum Thunb., Panax ginseng C.A. Mey, and Pueraria lobata (Willd.) Ohwi. Their active compounds, 2,3,4',5-Tetrahydroxystilbene-2-O-D-glucoside, ginsenoside Rb1, and puerarin, may act as the molecular substance for their anti-ARHL efficacy, and show anti-oxidative, neuroprotective, anti-inflammatory, anti-apoptotic, or mitochondrial protective effects. Conclusion Anti-oxidants, modulators of mitochondrial function, anti-inflammation agents, vasodilators, K+ channel openers, Ca2+ channel blockers, JNK inhibitors, and nerve growth factors/neurotrophic factors all contribute to hearing protection, and herbs are an important source of potential anti-ARHL drugs.

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Section: Pathophysiological Mechanisms and Treatment Strategies Of Arhlmentioning

confidence: 99%

Age-related hearing loss and its potential drug candidates: a systematic review

Hu,

Sun,

et al. 2023

Chin Med

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“…An imbalance of neurotrophic factors and their receptors has been reported for both AD and ARHL. In this context, nerve growth factor (NGF), GDNF and BDNF stand out [ 122 , 123 , 124 , 125 , 126 , 127 , 128 ]. The identified neurotrophic factors affected have been shown to have meaningful implications in the frame of neuronal degeneration processes.…”

Section: Neurotrophic Factors At the Interface Of Ad Pathophysiology ...mentioning

confidence: 99%

“…These therapies appear to be promising to protect or promote the regeneration of both hair cells and SGNs, thus regenerating or even preventing deafness of the mammalian inner ear [ 130 ]; meanwhile, they positively affect AD. However, their safety and efficacy in clinical studies are not yet proven [ 125 , 131 , 132 ]. Further future research and randomized clinical trials are warranted to examine and foster these implications of treatment for cognition and ARHL on a more profound level.…”

Section: Neurotrophic Factors At the Interface Of Ad Pathophysiology ...mentioning

confidence: 99%

Linking Cerebrovascular Dysfunction to Age-Related Hearing Loss and Alzheimer’s Disease—Are Systemic Approaches for Diagnosis and Therapy Required?

et al. 2022

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Alzheimer’s disease (AD), the most common cause of dementia in the elderly, is a neurodegenerative disorder associated with neurovascular dysfunction, cognitive decline, and the accumulation of amyloid β peptide (Aβ) in the brain and tau-related lesions in neurons termed neurofibrillary tangles (NFTs). Aβ deposits and NFT formation are the central pathological hallmarks in AD brains, and the majority of AD cases have been shown to exhibit a complex combination of systemic comorbidities. While AD is the foremost common cause of dementia in the elderly, age-related hearing loss (ARHL) is the most predominant sensory deficit in the elderly. During aging, chronic inflammation and resulting endothelial dysfunction have been described and might be key contributors to AD; we discuss an intriguing possible link between inner ear strial microvascular pathology and blood–brain barrier pathology and present ARHL as a potentially modifiable and treatable risk factor for AD development. We present compelling evidence that ARHL might well be seen as an important risk factor in AD development: progressive hearing impairment, leading to social isolation, and its comorbidities, such as frailty, falls, and late-onset depression, link ARHL with cognitive decline and increased risk of dementia, rendering it tempting to speculate that ARHL might be a potential common molecular and pathological trigger for AD. Additionally, one could speculate that amyloid-beta might damage the blood–labyrinth barrier as it does to the blood–brain barrier, leading to ARHL pathology. Finally, there are options for the treatment of ARHL by targeted neurotrophic factor supplementation to the cochlea to improve cognitive outcomes; they can also prevent AD development and AD-related comorbidity in the future.

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“…Furthermore, other neurotrophic factors were tested in animal models of hearing loss. For example, NGF or NT3 application prevents the OHC loss in mouse models of early-onset progressive hearing loss (78)(79)(80).…”

Section: Attenuation Of Outer Hair Cell Loss Without Functional Effec...mentioning

confidence: 99%

Pegylated Insulin-Like Growth Factor 1 attenuates Hair Cell Loss and promotes Presynaptic Maintenance of Medial Olivocochlear Cholinergic Fibers in the Cochlea of the Progressive Motor Neuropathy Mouse

Bieniussa

Kahraman²,

Skornicka³

et al. 2022

Front. Neurol.

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The progressive motor neuropathy (PMN) mouse is a model of an inherited motor neuropathy disease with progressive neurodegeneration. Axon degeneration associates with homozygous mutations of the TBCE gene encoding the tubulin chaperone E protein. TBCE is responsible for the correct dimerization of alpha and beta-tubulin. Strikingly, the PMN mouse also develops a progressive hearing loss after normal hearing onset, characterized by degeneration of the auditory nerve and outer hair cell (OHC) loss. However, the development of this neuronal and cochlear pathology is not fully understood yet. Previous studies with pegylated insulin-like growth factor 1 (peg-IGF-1) treatment in this mouse model have been shown to expand lifespan, weight, muscle strength, and motor coordination. Accordingly, peg-IGF-1 was evaluated for an otoprotective effect. We investigated the effect of peg-IGF-1 on the auditory system by treatment starting at postnatal day 15 (p15). Histological analysis revealed positive effects on OHC synapses of medial olivocochlear (MOC) neuronal fibers and a short-term attenuation of OHC loss. Peg-IGF-1 was able to conditionally restore the disorganization of OHC synapses and maintain the provision of cholinergic acetyltransferase in presynapses. To assess auditory function, frequency-specific auditory brainstem responses and distortion product otoacoustic emissions were recorded in animals on p21 and p28. However, despite the positive effect on MOC fibers and OHC, no restoration of hearing could be achieved. The present work demonstrates that the synaptic pathology of efferent MOC fibers in PMN mice represents a particular form of “efferent auditory neuropathy.” Peg-IGF-1 showed an otoprotective effect by preventing the degeneration of OHCs and efferent synapses. However, enhanced efforts are needed to optimize the treatment to obtain detectable improvements in hearing performances.

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Hearing Improvement in A/J Mice via the Mouse Nerve Growth Factor

Cited by 9 publications

References 23 publications

Age-related hearing loss and its potential drug candidates: a systematic review

Age-related hearing loss and its potential drug candidates: a systematic review

Linking Cerebrovascular Dysfunction to Age-Related Hearing Loss and Alzheimer’s Disease—Are Systemic Approaches for Diagnosis and Therapy Required?

Pegylated Insulin-Like Growth Factor 1 attenuates Hair Cell Loss and promotes Presynaptic Maintenance of Medial Olivocochlear Cholinergic Fibers in the Cochlea of the Progressive Motor Neuropathy Mouse

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