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Retina

High Correlation between Glaucoma Treatment with Topical Prostaglandin Analogs and BDNF Immunoreactivity in Human Retina

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Pages 739-745 | Received 09 Mar 2020, Accepted 06 Sep 2020, Published online: 27 Sep 2020
 

ABSTRACT

Purpose

To examine the expression of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, tropomyosin-related kinase receptor-B (TrkB), in normal and glaucomatous human retinas.

Methods

Human retinas were collected from 8 donors who had been clinically diagnosed and treated for glaucoma, and from 9 control donors. Immunohistochemical analysis for BDNF and TrkB was performed. The percent of each retina expressing BDNF and TrkB was quantified for the total retinal thickness, and separately for the retinal ganglion cell (RGC) complex + retinal nerve fiber layer (RNFL). The expression of each protein was correlated with clinical outcomes obtained from the subject’s ocular histories.

Results

There was no significant difference in BDNF or TrkB expression when comparing glaucomatous and control retinas. Correlation analysis revealed a significant relationship between BDNF expression and the use of prostaglandin analogs. TrkB expression was highly correlated with the last-measured intraocular pressure (IOP), the use of carbonic anhydrase inhibitors, the use of beta blockers, and the total number of drugs used for the treatment of glaucoma.

Conclusion

Topical drugs used to treat glaucoma were associated with an increase in retinal BDNF and TrkB expression in human retina, independent of IOP, which may represent molecular evidence of neuroprotective pathway activation.

Declaration of interest

The authors have no conflicts of interest to report.

Supplementary material

Supplemental data for this article can be accessed on the publisher’s website.

Additional information

Funding

This material is based upon work supported in part by the Department of Veterans Affairs [RX003002] and the United States National Institutes of Health [P30 EY025580]. The content of this manuscript is solely the responsibility of the authors and do not necessarily represent the official views of the granting agencies.

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