Correcting mitochondrial decline and improving retinal function – implications for AMD as it reduces inflammation
Professor Glen Jeffery
Professor of Neuroscience
Inst Ophthalmology – Visual Neuroscience Institute of Ophthalmology
Faculty of Brain Sciences
There is a growing body of evidence that the pace of aging is linked to metabolic rate, with high rates associated with faster aging (Speakman, 2005; Wang et al., 2010). Indeed, the retina is a key example of this as photoreceptors have the greatest energy demand in the body (Linsenmeier and Padnick-Silver, 2000). Experiments with mice have shown that mitochondria decline with age (Kokkinopoulos et al., 2013) and ATP the key sauce of cellular energy that they produce declines significantly by 3-4 months. Following these events, chronic inflammation becomes established (Catchpole et al., 2013; Hoh Kam et al., 2013; Xu et al., 2009), and retinal function declines (Kolesnikov et al., 2010; Li et al., 2001). It has been shown that there is a resulting 30% photoreceptor loss in both mouse and man (Cunea and Jeffery, 2007; Cunea et al., 2014; Curcio, 2001).
Supported by this recent body of research evidence, Professor Glen Jeffery and his team are showing that some of these features in the ageing retina can be corrected, based on the principle that specific long wave- lengths of light absorbed by cytochrome c oxidase (Fitzgerald et al., 2013), which is a key element in mitochondrial provision of ATP. Experiments with mice expose to long wavelength light (670nm) have shown that retinal inflammation is reduced and retinal function improved by around 25% when the physiological function of the mouse eye is examined. The mitochondrial membranes recharge and more ATP is available for cellular function. So, Glen Jeffery’s data suggest, 670 nm light can significantly improve aged retinal function, perhaps by providing additional ATP for the energy demanding cellular pumps that all neuronal cells have and this extra energy is associated with a reduction in the chronic level of inflammation that the ageing retina suffers from. This relatively simple therapeutic route may have significant implications for the preventative treatment of early AMD prior to the onset of dry AMD (geographic atrophy) and retinal aging.
Perhaps as importantly, Glen Jeffery’s laboratory has been able to monitor mitochondrial function in the living eye via reflected light (Kaynezhad et al 2016) and consequently they may be able to identify those in which the function is being undermined at a relatively rapid rate, and as such be vulnerable to disease.
Glen Jeffery’s research is supported by the Biotechnological and Biological Research Council UK.