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Editors Selection IGR 16-3

Basic Science: Mitochondrial-mediated Neuroprotection

Comment by Miriam Kolko on:

73163 Topical Coenzyme Q10 demonstrates mitochondrial-mediated neuroprotection in a rodent model of ocular hypertension, Davis BM; Tian K; Pahlitzsch M et al., Mitochondrion, 2017; 36: 114-123

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In the present study, the authors elucidate the potential neuroprotective role of coenzyme Q10 (coQ10). CoQ10 is known as an antioxidant. Moreover, coQ10 carries electrons between complex I and III and complex II and III in the oxidative phosphorylation. Since emerging studies have related mitochondrial dysfunction and glaucomatous loss of retinal ganglion cells (RGCs), it is likely that treatments to support the electron transport and thereby increase ATP production and reduce the production of reactive oxygen species (ROS) may rescue the RGCs and their axons.

The study provides supportive evidence of CoQ10/TPGS as a neuroprotective treatment and emphasizes a great potential of the "Detection of apoptosing retinal cells"

Since previous studies have proven better delivery of coQ10 when combined with the vitamin E derivative D-α-Tocopherol polyethylene glycol 1000 succinate (TPGS), the authors used this combined treatment to investigate the neuroprotective properties of coQ10. The authors reported that topically instilled CoQ10/TPGS micelles were delivered in neuroprotective concentrations to the retina. In order to investigate the protective efficacy of CoQ10/TPGS, the authors used primary murine retinal mixed cultures and the immortalized retinal photoreceptor cell line (RGC5). Moreover, an in vivo Morrison's model of ocular hypertension was used. To induce mitochondrial impairment cells were exposed to DMSO and paraquat. Whereas both DMSO and paraquat induce oxidative stress, paraquat has furthermore been shown to reduce complex I activities. In both mixed murine retinal cultures, RGC5 and in the ocular hypertension model, the authors reported neuroprotective effects of CoQ10/TPGS.

While the results are interesting and supporting previous findings of CoQ10 as a possible neuroprotective agent, an important consideration is how generalizable the results are to glaucoma. Moreover, the particular impact of the oxidative phosphorylation complexes and/or ROS production in the pathophysiology of glaucoma is still debated and future studies would benefit from more stringent measurements of the various complex activities compared to ROS production in response to CoQ10/TPGS. In spite of the need for extended studies to investigate the potential use of CoQ10/TPGS to prevent progressive glaucomatous RGC loss, the study provides supportive evidence of CoQ10/TPGS as a neuroprotective treatment and emphasizes a great potential of the "Detection of apoptosing retinal cells", DARC technique as a tool to monitor the efficacy of potential neuroprotective treatments.

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