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Glaucoma Dialogue IGR 15-1

Response

Comment by Lin Wang on:

53854 Longitudinal hemodynamic changes within the optic nerve head in experimental glaucoma, Cull G; Burgoyne CF; Fortune B et al., Investigative Ophthalmology and Visual Science, 2013; 54: 4271-4277

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We would like to thank Drs. Harris, Pasquale and Schmetterer for their insightful comments about our recent article, 'Longitudinal Hemodynamic Changes within the Optic Nerve Head in Experimental Glaucoma'. The role of blood flow insufficiency in the development of glaucomatous optic neuropathy has been a topic of discussion for a long time. Questions, such as whether reduced blood flow in the optic nerve head is associated with increased IOP or independently as a primary insult in human glaucoma, as pointed out in the comments, still remain unclear. We entirely agree with the comments that although the study of this high IOP glaucoma model reveals a twophase patterned blood flow change and a close relationship between the blood flow and retinal nerve fiber layer thickness, further investigation is necessary to validate this observation in human glaucoma. Investigations are ongoing to quantify the static and dynamic autoregulation capacity for blood flow in the optic nerve head (ONH) of non‐human primates with experimental glaucoma and we have begun initial investigations to quantify ONH blood flow autoregulation in healthy human subjects. In addition, as part of this series of studies, we are planning to revisit our animal model to examine the blood flow in a non-pressure induced optic neuropathy (optic nerve transection) similar to suggestion offered in Comment 1. We anticipate that these experiments collectively will provide additional insight about the physiological mechanism underlying hemodynamic changes observed in glaucoma.

The proposed genetic cause and the role of glial cells in the systemic vascular dysregulation mentioned in Comment 2 are very interesting. In parallel to our in‐vivo studies, we are currently utilizing proteomics and immunohistological techniques to identify potential biomarkers within the optic nerves and retinas at different stages of experimental glaucoma; we are also developing both in‐vivo and ex-vivo methods to investigate the role of glial cells in the pathological mechanisms leading to compromised blood flow. We hypothesize that following chronic, moderate IOP elevation, early disruption of the autoregulation system occurs and manifests as either an increase or decrease in blood flow via dysfunction of the glia‐vascular unit. Identifying the mechanisms of this dysfunction and its stabilization may yield the optic nerve head targets for neuroprotection.

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