Showing papers by "Marlan R. Hansen published in 2007"
TL;DR: Four among five small studies indicate that administration of zinc has a beneficial effect on tinnitus but these results still have to be confirmed in clinical trials with larger samples using a cross-over design, validatedTinnitus handicap questionnaires, measurements of tinnitis magnitude, and accessing the coexistence of other symptoms such as depression, phonophobia, and hyperacusis.
Abstract: Zinc is an essential trace element present in all organs, tissues, fluids, and secretions of the body and it is widely distributed in the central nervous system, including the auditory pathway in synapses of the VIII nerve and in the cochlea Zinc is an essential component of Cu/Zn superoxide dismutase (SOD) and in certain enzymes and it is important for proper function of the immune system Three possible mechanisms have linked zinc to tinnitus; cochlear Cu/Zn SOD activity, synaptic transmission, and depression Evidences in the literature suggest prevalence rates of zinc deficiency in individuals with tinnitus from 2 to 69%, affecting elderly individuals more frequently Four among five small studies indicate that administration of zinc has a beneficial effect on tinnitus but these results still have to be confirmed in clinical trials with larger samples using a cross-over design, validated tinnitus handicap questionnaires, measurements of tinnitus magnitude, and accessing the coexistence of other symptoms such as depression, phonophobia, and hyperacusis
25 citations
TL;DR: Although overexpression of prosurvival members of the Bcl‐2 family prevents SGN loss following trophic factor deprivation, the inhibition of neurite growth by these molecules may limit their efficacy for support of auditory nerve maintenance or regeneration following hair cell loss.
Abstract: Spiral ganglion neurons (SGNs) provide afferent innervation to the cochlea and rely on contact with hair cells (HCs) for their survival. Following deafferentation due to hair cell loss, SGNs gradually die. In a rat culture model, we explored the ability of prosurvival members of the Bcl-2 family of proteins to support the survival and neurite outgrowth of SGNs. We found that overexpression of either Bcl-2 or Bcl-xL significantly increases SGN survival in the absence of neurotrophic factors, establishing that the Bcl-2 pathway is sufficient for SGN cell survival and that SGN deprived of trophic support die by an apoptotic mechanism. However, in contrast to observations in central neurons and PC12 cells where Bcl-2 appears to promote neurite growth, both Bcl-2 and Bcl-xL overexpression dramatically inhibit neurite outgrowth in SGNs. This inhibition of neurite growth by Bcl-2 occurs in nearly all SGNs even in the presence of multiple neurotrophic factors implying that Bcl-2 directly inhibits neurite growth rather than simply rescuing a subpopulation of neurons incapable of extending neurites without additional stimuli. Thus, although overexpression of prosurvival members of the Bcl-2 family prevents SGN loss following trophic factor deprivation, the inhibition of neurite growth by these molecules may limit their efficacy for support of auditory nerve maintenance or regeneration following hair cell loss. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007
24 citations