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M. M. Harper, L. M. Eggers, M. H. Kuehn, D. S. Sakaguchi, R. H. Kardon, S. D. Grozdanic; Quantification and Correlation of Neurotrophic Factor Expression With Medical Histories in Healthy and Glaucomatous Tissue. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2112.
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To quantify the expression of brain-derived neurotrophic factor (BDNF) and the TrkB receptor in glaucomatous and normal human retinas. We also sought to correlate the expression of the proteins with parameters collected from patient medical histories.
Human glaucomatous retinas (n=8) were collected from patients with clinically diagnosed primary glaucoma. Healthy retinas (n=9) were collected to serve as a control. Immunohistochemical analysis for BDNF and its receptor (TrkB) were performed using permanent staining techniques and quantified. Regression analysis was used to correlate protein expression with visual parameters (visual acuity, refraction, cup/disk ratio), intraocular pressure and the medical treatment (type of drug, number of drugs).
Overall, there was not a significant difference in BDNF (p=0.1487, Student’s t-test) or TrkB (p=0.5759) expression between healthy and glaucomatous retinas. However, TrkB expression in glaucomatous tissue was negatively correlated with the IOP (r2=0.9901, p=0.0004) and was positively correlated with the use of beta blockers (r2=0.8143, p=0.0054) and carbonic anhydrase inhibitors (CAI) (r2=0.5851, p=0.0451). BDNF expression in glaucomatous tissue was positively correlated with the use of prostaglandin (PG) analogs (r2=0.752, p=0.0053), but not correlated with other evaluated parameters.
This study has systematically examined BDNF and TrkB expression in patients suffering from primary glaucoma. We have demonstrated that retinal protein expression could be affected by IOP levels (TrkB) and the medical treatment with specific drugs (BDNF-PG, TrkB- beta blockers and CAI). The type and number of drugs used for medical treatment did not correlate with IOP suggesting that the observed expression of TrkB and BDNF may be the result of a direct effect of drugs on the retina, rather than the pharmacological effect on the IOP itself.
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