Expression pattern of brain-derived neurotrophic factor and its associated receptors: Implications for exogenous neurotrophin application

Schulze, Jessika; Staecker, Hinrich; Wedekind, Dirk; Lenarz, Thomas; Warnecke, Athanasia

doi:10.1016/j.heares.2020.108098

Cited by 16 publications

(7 citation statements)

References 66 publications

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“…However, no immunoreactivity of the stria vascularis or hair cells was observed (Despres et al., 1991 ). In adult rodents, it was reported that NGFR was expressed in the majority of the neurons in the spiral ganglion as well as the pillar and supporting cells around the outer hair cells (Schulze et al., 2020 ). In humans, a broad expression of NGFR is observed in the adult inner ear in neurons, Schwann and satellite cells in the spiral ganglion, as well as in hair cells and supporting cells in the organ of Corti (Johnson Chacko et al., 2017 ; Liu et al., 2012 ), and the expression of NGFR in the spiral ganglion in early phase fetuses (GW11) has also been reported (Johnson Chacko et al., 2017 ).…”

Section: Resultsmentioning

confidence: 99%

Neuronal development in the cochlea of a nonhuman primate model, the common marmoset

Fujioka

Murayama

Ozawa

et al. 2021

Developmental Neurobiology

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Precise cochlear neuronal development is vital to hearing ability. Understanding the developmental process of the spiral ganglion is useful for studying hearing loss aimed at aging or regenerative therapy. Although interspecies differences have been reported between rodents and humans, to date, most of our knowledge about the development of cochlear neuronal development has been obtained from rodent models because of the difficulty in using human fetal samples in this field. In this study, we investigated cochlear neuronal development in a small New World monkey species, the common marmoset (Callithrix jacchus). We examined more than 25 genes involved in the neuronal development of the cochlea and described the critical developmental steps of these neurons. We also revealed similarities and differences between previously reported rodent models and this primate animal model. Our results clarified that this animal model of cochlear neuronal development is more similar to humans than rodents and is suitable as an alternative for the analysis of human cochlear development. The time course established in this report will be a useful tool for studying primate‐specific neuronal biology of the inner ear, which could eventually lead to new treatment strategies for human hearing loss.

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Section: Resultsmentioning

confidence: 99%

Neuronal development in the cochlea of a nonhuman primate model, the common marmoset

Fujioka

Murayama

Ozawa

et al. 2021

Developmental Neurobiology

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“…Comparably, common microvascular pathology has been proposed to be at the root of diabetes-associated complications involving the microvasculature of eyes, heart and kidneys, respectively [ 98 , 99 , 100 ]. Our hypothesis, linking AD genesis to ARHL, is further strengthened by the fact that many cerebrovascular diseases are associated with frailty; for example, stroke, congestive heart failure, and diabetes-associated complications seem to include cognitive impairment and disturbances in hearing as comorbidities [ 101 ].…”

Section: Age-related Hearing Loss In the Genesis Of Admentioning

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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“…Some growth factors and neurotrophins, such as fibroblast growth factor (FGF), BDNF, glial cell-derived neurotrophic factor (GDNF), and NT-3, play important roles during SGNs development and survival (Johnson Chacko et al, 2017 ). Treatment of mature BDNF and proBDNF in SGNs cultures with a concentration as low as ng/ml-range could exert a protective effect on SGNs against degeneration (Schulze et al, 2020 ). Previous studies also found that FGF, GDNF, and NT-3 promoted the outgrowth of neurites from cultured SGNs, which indicated that these molecules may also have trophic functions in SGNs regeneration (Wei et al, 2007 ; Wang and Green, 2011 ; Garcia-Hernandez et al, 2013 ).…”

Section: Neurotrophic Factors and Signaling Pathways Enhance The Sgns Regenerationmentioning

confidence: 99%

Regulation of Spiral Ganglion Neuron Regeneration as a Therapeutic Strategy in Sensorineural Hearing Loss

Wang

Han

et al. 2022

Front. Mol. Neurosci.

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In the mammalian cochlea, spiral ganglion neurons (SGNs) are the primary neurons on the auditory conduction pathway that relay sound signals from the inner ear to the brainstem. However, because the SGNs lack the regeneration ability, degeneration and loss of SGNs cause irreversible sensorineural hearing loss (SNHL). Besides, the effectiveness of cochlear implant therapy, which is the major treatment of SNHL currently, relies on healthy and adequate numbers of intact SGNs. Therefore, it is of great clinical significance to explore how to regenerate the SGNs. In recent years, a number of researches have been performed to improve the SGNs regeneration strategy, and some of them have shown promising results, including the progress of SGN regeneration from exogenous stem cells transplantation and endogenous glial cells’ reprogramming. Yet, there are challenges faced in the effectiveness of SGNs regeneration, the maturation and function of newly generated neurons as well as auditory function recovery. In this review, we describe recent advances in researches in SGNs regeneration. In the coming years, regenerating SGNs in the cochleae should become one of the leading biological strategies to recover hearing loss.

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Expression pattern of brain-derived neurotrophic factor and its associated receptors: Implications for exogenous neurotrophin application

Cited by 16 publications

References 66 publications

Neuronal development in the cochlea of a nonhuman primate model, the common marmoset

Neuronal development in the cochlea of a nonhuman primate model, the common marmoset

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

Regulation of Spiral Ganglion Neuron Regeneration as a Therapeutic Strategy in Sensorineural Hearing Loss

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