COMMENTARY

Keep an 'Eye' on Curcumin for Ocular Neuroprotection

Brianne N. Hobbs, OD

Disclosures

August 29, 2018

Neuroprotection is alluring. The ability to actually increase the resiliency of delicate central nervous system structures, including the optic nerve, would be huge step forward in the management of glaucoma and other neurodegenerative diseases.

Several compounds have demonstrated this desired neuroprotective quality, but the incorporation of these compounds into clinical practice lags owing to a variety of issues. Curcumin, the main active ingredient in turmeric, is one such substance and has previously been shown to have promise in neurodegenerative ocular disease.[1] Unfortunately, clinical utility has been limited because curcumin has proven difficult to formulate into an effective eye drop, owing to its low solubility and poor bioavailability.

The gap between promising neuroprotectant and feasible therapeutic option was recently narrowed by Davis and colleagues,[2] who set out to develop a novel method of formulating a topical administration of curcumin. The delivery system was then tested to ensure that the active properties of the compound were maintained.

Davis and colleagues also investigated whether this curcumin delivery system was effective in protecting retinal ganglion cells in two established in vivo rodent models simulating ocular hypertension and partial optic nerve transection. The rats in the study received two drops of curcumin-loaded nanocarriers every day for 3 weeks beginning 2 days before the simulated optic nerve injury. The density of retinal ganglion cells was then compared between the control group and the curcumin treatment group to assess the degree of any potential neuroprotective effect.

A highly soluble, stable, and readily bioavailable delivery system for curcumin was successfully created by this team. The creation of curcumin-loaded nanocarriers preserved the neuroprotective effects of curcumin in the convenience of an eye drop. The topical administration was seemingly well-tolerated, with no signs of ocular irritation or inflammation.

In both rodent models of retinal ganglion cell loss, there was significant preservation of the retinal ganglion cell density in the curcumin treatment group. In the ocular hypertension rodent model, there was no significant difference in intraocular pressure (IOP) between the curcumin and control groups, thus demonstrating that curcumin does not exhibit its neuroprotective effect by lowering IOP.

Taken together, the results of this trial are threefold:

  1. Curcumin was formulated into an effective topical delivery system.

  2. Neuroprotective activity of curcumin was confirmed in vitro and in vivo.

  3. Retinal ganglion cell density was significantly preserved in two models of ocular injury.

The application of the topical curcumin began 2 days before nerve injury; it is difficult to know what effect this pretreatment had on outcomes. It is possible that the neuroprotective effect would have been dramatically decreased or eliminated without this early dosing. If future studies confirm application before injury is necessary for neuroprotection, then curcumin may still be useful clinically in patients undergoing procedures known to cause IOP spikes or by patients who are at very high risk for glaucoma, as the authors suggest.

The real advance of this trial was not in proving the neuroprotective activity of curcumin (which had previously been established), but rather in harnessing its power and translating it to clinical relevance. Before the topical formulation was developed, the oral dosage of curcumin necessary to induce an effect previously was estimated to be up to twenty-four 500-mg tablets daily- an amount that precluded its use clinically owing to adverse effects. This nanocarrier delivery system will make a daily topical application of curcumin a viable option if it is shown to be effective in humans.

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