Age related macular degeneration (AMD) is the largest cause of aged blindness in those over 60 years. This slowly progressive disease, where the central retina is lost, is associated with inflammatory deposition, reduced mitochondrial function and cell loss. In 50% of patients there is a problem with a gene associated with immunity.

In disease models with the same genetic deficit the disease does not develop when the models are kept in a pathogen free environment and their immunity is not challenged. This strongly implies that, in these models, there are interactions between the environment and a predisposition for disease development that has implications for patients. 

Professor Glen Jeffery and his team at UCL will explore the relationship between the environment and immune vulnerability in a disease model focusing on key sub-cellular structures known as mitochondria. Mitochondria provide energy for cells, but also regulate ageing, inflammation, and cell death. Mitochondrial failure has been implicated in AMD development both in patients and disease models.

The research will look for the vulnerability in the model in both clean models and those exposed to an open environment containing common pathogens. This will involve examining arrays for a wide range of markers of mitochondrial function and inflammation in both the retina and also in the blood. 

Once a baseline is established, the team will move clean models into an open environment at progressive stages and re-examine these features to determine when and how the environment imposes itself on the retina and what changes are associated with the move that start off the disease process. Conversely, once disease has been initiated by environmental exposure, the researchers will test if placing the models in a clean environment can arrest pathological development.  This may have significant consequences for patients if reduced pathogen exposure, via flu inoculation for instance, can impact on AMD.

Previously, little attention has been paid to the role of the environment and its pathogens as potential drivers of AMD. In part this is because disease development is slow and human environmental exposure is complex and varied. This highlights the importance of using this established model to unravel environmental influences on AMD development.

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