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Editors Selection IGR 18-1

Basic Science: Neuroprotection

Comment by Keith Martin on:

77097 Structural and Functional Rescue of Chronic Metabolically Stressed Optic Nerves through Respiration, Harun-Or-Rashid M; Pappenhagen N; Palmer PG et al., Journal of Neuroscience, 2018; 38: 5122-5139

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The importance of metabolic stress as a contributing factor to retinal ganglion cell (RGC) loss in optic nerve diseases such as glaucoma has been highlighted in numerous recent studies. A key question is whether energy substrate availability or mitochondrial dysfunction contributes to the energy compromise observed in glaucoma.

The current study adds to a growing body of literature on the potential benefits of dietary modification

To test this idea, Harun-Or-Rashid and co-workers placed DBA/2J mice (which develop a form of pigmentary glaucoma as they age) and control mice on a ketogenic diet composed primarily of fat in order to promote mitochondrial biogenesis and compel mitochondrial respiration through utilization of ketone bodies rather than glucose. They found that eight weeks of the diet generated increased numbers of mitochondria, improved energy availability, reduced glial hypertrophy and protected RGC and their axons from degeneration.

The experiments appear to have been carefully performed and it is of interest that similar metabolic changes were also observed in a microbead model of glaucoma as well as in the DBA/2J mice. In previous studies by other groups, caloric restriction by alternate day fasting has been shown to improve RGC survival and function in a mouse model of normal tension glaucoma. Ketogenic diets have also been shown to reduce neurodegeneration in models of Alzheimer's disease. The current study therefore adds to a growing body of literature on the potential benefits of dietary modification in animal models of glaucoma and the results of future human clinical trials are awaited with interest.

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