Scientists from the University of Wisconsin at Madison published in the journal eLife, a study which shows that a protein known as Transmembrane 135 regulates the aging of the retina, and that mutations in the protein can lead to disease.
The study was conducted on mice, and showed that abnormal amounts of Tmem135 leads to symptoms of a common retinal disease which develops in the older population, known as macular degeneration.
“Age-related macular degeneration (AMD), which affects roughly 11 million people in the US alone, usually leads to loss of central vision — what you see when you look straight ahead — in both eyes. The vision becomes more blurred as time goes on, making it more difficult to read and even recognize people,” says senior author Akihiro Ikeda and Professor Walter H. Helmerich of the McPherson Eye Research Institute at the University of Wisconsin-Madison.
“There is currently no cure for AMD, of which there are two types: wet AMD and dry AMD, and no proven medical treatment is available for dry AMD which affects about 90% of overall patients. Our study presents Tmem135, or the consequences of its defect, as potential new therapy targets for AMD and similar retinal conditions that occur later in life.”
Using genetic mapping of the mice which exhibited symptoms of retinal abnormalities, the team was able to discover that Tmem135 is linked to these irregularities. They then found that the protein controls the size of the mitochondria in the effected cells, leading to abnormalities in the metabolic functions of the cells.
“The regulation of mitochondrial size by Tmem135 determines the sensitivity of cells to environmental stress and the pace of aging in the retina,” says first author Wei-Hua Lee. “On the other hand, mutations lead to higher sensitivity to such stress, showing that the protein is critical for protecting against this and for controlling the progression of retinal aging.
“Overall, the fact that a single mutation leads to both accelerated aging and causes age-dependent disease symptoms in mice confirms that these processes are closely associated with each other at the molecular level. Based on our findings, Tmem135 may be a key molecule that could tip the normal aging process toward age-dependent diseases and potentially be explored for future treatments.”
The scientists will now try to find out the exact biochemical and molecular functions controlled by Tmem135 and look at its role in the aging of other tissues and other age-dependent illnesses.
