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Ganglion Cell Loss (ganglion + cell_loss)
Selected AbstractsSubunits of the epithelial sodium channel family are differentially expressed in the retina of mice with ocular hypertensionJOURNAL OF NEUROCHEMISTRY, Issue 1 2005Frank M. Dyka Abstract Glaucoma is a prevalent cause of blindness, resulting in the apoptotic death of retinal ganglion cells and optic nerve degeneration. The disease is often associated with elevated intraocular pressure, however, molecular mechanisms involved in ganglion cell death are poorly understood. To identify proteins contributing to this pathological process, we analysed the retinal gene expression of DBA/2J mice that develop an elevated intraocular pressure by the age of 6 months with subsequent ganglion cell loss. In this study, we identified subunits of the epithelial sodium channel (ENaC) family that are specifically expressed under elevated intraocular pressure. Using reverse transcriptase polymerase chain reaction we observed a significant increase of ,-ENaC in the neuronal retina of DBA/2J mice when compared with control animals, while ,-ENaC and ,-ENaC were not detectable in this tissue. Specific immune sera to ENaC subunits showed up-regulation of ,-ENaC in synaptic and nuclear layers of the retina, and in the retinal pigment epithelium. Consistent with our polymerase chain reaction data, ,-ENaC was not detected by specific antibodies in the retina, while ,-ENaC was only present in the retinal pigment epithelium under ocular hypertension. Finally, the increase of ,-ENaC gene expression in the neuronal retina and the retinal pigment epithelium was not observed in other tissues of DBA/2J mice. Since the intraocular pressure is regulated by the transport of aqueous humour across epithelial structures of the eye that in turn is associated with ion flux, the specific up-regulation of ENaC proteins could serve as a protecting mechanism against elevated intraocular pressure. [source] Presbycusis: A Human Temporal Bone Study of Individuals With Downward Sloping Audiometric Patterns of Hearing Loss and Review of the LiteratureTHE LARYNGOSCOPE, Issue S112 2006Erik G. Nelson MD Abstract Objective: The purpose of this retrospective case review was to identify patterns of cochlear element degeneration in individuals with presbycusis exhibiting downward sloping audiometric patterns of hearing loss and to correlate these findings with those reported in the literature to clarify conflicting concepts regarding the association between hearing loss and morphologic abnormalities. Methods: Archival human temporal bones from individuals with presbycusis were selected on the basis of strict audiometric criteria for downward-sloping audiometric thresholds. Twenty-one temporal bones that met these criteria were identified and compared with 10 temporal bones from individuals with normal hearing. The stria vascularis volumes, spiral ganglion cell populations, inner hair cells, and outer hair cells were quantitatively evaluated. The relationship between the severity of hearing loss and the degeneration of cochlear elements was analyzed using univariate linear regression models. Results: Outer hair cell loss and ganglion cell loss was observed in all individuals with presbycusis. Inner hair cell loss was observed in 18 of the 21 individuals with presbycusis and stria vascularis loss was observed in 10 of the 21 individuals with presbycusis. The extent of degeneration of all four of the cochlear elements evaluated was highly associated with the severity of hearing loss based on audiometric thresholds at 8,000 Hz and the pure-tone average at 500, 1,000, and 2,000 Hz. The extent of ganglion cell degeneration was associated with the slope of the audiogram. Conclusions: Individuals with downward-sloping audiometric patterns of presbycusis exhibit degeneration of the stria vascularis, spiral ganglion cells, inner hair cells, and outer hair cells that is associated with the severity of hearing loss. This association has not been previously reported in studies that did not use quantitative methodologies for evaluating the cochlear elements and strict audiometric criteria for selecting cases. [source] 2153: Can we treat glaucoma by non-IOP related approaches?ACTA OPHTHALMOLOGICA, Issue 2010I STALMANS Intra-ocular pressure is the main risk factor for the progression of glaucoma. However, intra-ocular pressure lowering is not always sufficient to halt the progressive ganglion cell loss. Indeed, additional risk factors have been identified for glaucoma progression that can explain why some patients progress despite rigourous intra-ocular pressure lowering. Vascular risk factors, such as low perfusion pressure, can be taken into account in the management of our glaucoma patients. The treatment options for these vascular risk factors will be discussed during the lecture. Moreover, neuroprotective strategies might open therapeutic perspectives to directly support the ganglion cells and thus help stabilizing the disease. Possible neuroprotective agents will be highlighted. [source] Choroidal blood flow and retinal ganglion cell function in early glaucomaACTA OPHTHALMOLOGICA, Issue 2009D MARANGONI Purpose To assess subfoveal choroidal blood flow in patients with early manifest glaucoma (EMG) and to compare blood flow with functional measures of retinal ganglion cell (RGC) integrity. Methods Subfoveal choroidal blood flow was determined by confocal, real-time laser Doppler flowmetry in 25 EMG patients (<-6 dB Humphrey mean deviation, age range: 42-64 years, visual acuity: 0.8-1.0) and in 20 age-matched controls. All patients had a therapeutically (topical beta-blockers with or without a prostaglandin) controlled intraocular pressure (IOP <20 mmHg). Subfoveal choroidal blood volume (ChBVol), velocity (ChBVel) and flow (ChBF) were determined as the average of three 60 sec recordings with changes in the DC < 10% between the recordings (DC measures the intensity of the light scattered by the tissue and red blood cells in the illuminated volume). In all patients and controls pattern electroretinograms (PERGs) were recorded according to a standardized protocol. Results In EMG patients, average ChBVel and ChBF were reduced by 31 and 35%, respectively (p <0.01) compared to control values. No significant difference in ChBVol was found between the two groups. PERG amplitudes were reduced by 40% (p <0.01) in EMG patients compared to controls. No correlation was found between anyone of the choroidal flow parameters and PERG data or IOP values. Conclusion The results suggest a significant alteration of subfoveal choroidal hemodynamics in EMG patients, involving both ChBVel and ChBF. These changes do not appear to be associated with the severity of functional retinal ganglion cell loss. Our findings may have implications for the pathophysiology of early glaucomatous damage and its treatment. [source] Scaling the structure,function relationship for clinical perimetryACTA OPHTHALMOLOGICA, Issue 4 2005Ronald S. Harwerth Abstract. Purpose:,The full ranges of glaucomatous visual field defects and retinal ganglion cell losses extend over several orders of magnitude and therefore an interpretation of the structure,function relationship for clinical perimetry requires scaling of both variables. However, the most appropriate scale has not been determined. The present study was undertaken to compare linear and logarithmic transformations, which have been proposed for correlating the perimetric defects and neural losses of glaucoma. Methods:,Perimetry, by behavioural testing, and retinal histology data were obtained from rhesus monkeys with significant visual field defects caused by experimental glaucoma. Ganglion cell densities were measured in histologic sections of retina that corresponded to specific perimetry test locations for the treated and control eyes. The linear (percentage) and logarithmic (decibel) relationships for sensitivity loss as a function of ganglion cell loss were analysed. Results:,With decibel scaling, visual sensitivity losses and ganglion cell densities were linearly correlated with high coefficients of determination (r2), although the parameters of the functions varied with eccentricity. The structure,function relationships expressed as linear percentage-loss functions were less systematic in two respects. Firstly, the relationship exhibited considerable scatter in the data for small losses in visual sensitivity and, secondly, visual sensitivity losses became saturated with larger losses in ganglion cell density. The parameters of the percentage-loss functions also varied with eccentricity, but the variation was less than for the decibel-loss functions. Conclusions:,Linear scaling of perimetric defects and ganglion cell losses might potentially improve the structure,function relationship for visual defects associated with small amounts of cell loss, but the usefulness of the relationship is limited because of the high variability in that range. With log,log co-ordinates, the structure,function relationship for clinical perimetry is relatively more accurate and precise for cell losses greater than about 3 dB. The comparatively greater accuracy and precision of decibel loss functions are a likely consequence of the logarithmic scale of stimulus intensities for perimetry measurements and because the relationship between visual sensitivity and the number of neural detectors is a form of probability summation. [source] | ||||||||||