A study recently published in the journal Neurobiology of Aging revealed that the degeneration of the eye’s retina is linked to a mitochondrial dysfunction. The study is entitled “Mitochondrial decline precedes phenotype development in the complement factor H mouse model of retinal degeneration but can be corrected by near infrared light,” and was conducted by researchers at the Federal Fluminense University in Brazil, as well as at the University College London and Moorfields Eye Hospital in the United Kingdom.
In the body, the eye’s outer retina is the entity with the greatest metabolic demand, which explains its high concentration of mitochondria in photoreceptors. Mitochondria are small organelles considered the powerhouses of the cells where the energy for the body is produced in the form of adenosine triphosphate (ATP). ATP is crucial for cellular metabolism.
As individuals age, the number of mutations in mitochondrial DNA increases, as well as the production of harmful pro-inflammatory reactive oxygen species (ROS), while the production of ATP decreases. This change in the equilibrium of mitochondrial function is linked to chronic inflammation and tissue degradation.
Retina also ages, leading to progressive inflammation and ultimately retinal cell loss. A compromised mitochondrial function has been suggested to be associated with the age-related macular degeneration (AMD), the deterioration of the eye’s macula (the part of the retina responsible for central vision that allows the clear perception of fine details).
In the study, researchers investigated the link between aging and retinal ATP levels using two mouse models, one with normal aging eyes and an AMD mouse model with the complement factor H depleted (CFH). CFH plays an important role in regulating the complement system, a part of the body’s immune response that helps in the elimination of foreign invaders. CFH depletion in mice mimics in part the AMD phenotype in humans.
Researchers found that mice without CFH suffer a premature decline of 30% in retinal ATP levels in comparison to normal mice. In addition, a shift towards the expression of the predominately mitochondrial heat shock protein 60 (Hsp60) is also observed in mice with CFH depleted. Hsp60 expression is usually linked to stress conditions and neuroprotection. Hsp60 helps proteins to achieve a proper folding and is involved in the replication and transmission of mitochondrial DNA. The ATP levels in the brain did not differ between the two mouse models.
It has been previously reported that exposure to near infrared light increases ATP levels and reduces inflammation. Interestingly, exposure of mice without CFH to near infrared light corrected the premature retinal ATP decline and shifted the Hsp60 expression pattern.
The research team concluded that AMD in mice is most likely linked to a mitochondrial dysfunction, and that the decline in ATP levels precedes outer retinal inflammation and cell loss. The team suggests that ATP decline could potentially be corrected by simply improving the mitochondrial function through near infrared light exposure.