Posted on Dec 06, 2016, 6 a.m.
The discovery of Tmem135 could lead to the development of new treatments for conditions causing sight loss in later life.
Scientists have discovered a new protein that links aging with age-related retinal diseases. This could lead to new therapies for eyesight loss in older people. In an article published in the journal eLife, researchers from the University of Wisconsin-Madison studied lab mice and found a protein called Tmem135 (Transmembrane 135) which is responsible for retinal aging. They discovered that mutations of this protein resulted in age-related retinal disease.
Millions Suffer Age-Related Retinal Diseases
Ironically, previous studies show that Tmem135 is associated with fat storage and extended life in a type of roundworm called Caenorhabditis Elegans. The molecular function of protein Tmem135 in the worms has yet to be determined. In the new study, researchers showed that irregular levels of this protein are linked to symptoms of macular degeneration, a common age-dependent retinal disease.
About 11 million people in the United States are afflicted with AMD (Age-related macular degeneration) which affects central vision in both eyes. The condition worsens as time passes, making it more difficult to see things, and there is no cure for this disease. There are two types of AMD: wet and dry, with dry affecting 90% of those with AMD. There are no scientifically proven treatments available. But researchers in the study have linked Tmem135 or its defect as a target for new medical treatments for people suffering retinal conditions.
Tmem135 May Lead to Future Retinal Treatments
How the team discovered Tmem135 is interesting. They used existing mouse models that matched similar retinal abnormalities that are found in mice that have early onset of retinal disease. The lab mice had their genes mapped which revealed a mutation in the protein Tmem135 thought to be the cause of the retinal conditions. Another discovery by the team of researchers was that the protein had a role in regulating size in the mitochondria in cells, thus determining the pace of aging in the retina. Also, it was shown that Tmem135 is critical for protecting cells against mutations further slowing down retinal aging.
The protein Tmem135 can mutate leading to accelerated age-related aging in the retina of mice. Its other role as a regulator of the mitochondria of cells, confirms the two processes are molecularly related to each other. The study concluded that Tmem135 is a key protein that needs further exploration to be potentially used in future treatments for humans. The research team is now working to determine the exact biochemical function of protein Tmem135 in cell mitochondria. Further examination is also needed to determine the role it has in changing the aging process in various tissues and other age-related diseases.
The paper 'Mouse Tmem135 mutation reveals a mechanism involving mitochondrial dynamics leading to age-dependent retinal pathologies' can be freely accessed online at http://dx.doi.org/10.7554/eLife.19264. Contents, including text, figures, and data, are free to reuse under a CC BY 4.0 license.