Researchers have identified a protein in our brain that keeps us young by preventing the breakdown of our DNA.
They believe the decay of that protein, called SIRT6, is linked to Alzheimer’s disease, Parkinson’s disease, and the rare neurological disease ALS (amyotrophic lateral sclerosis).
Dr. Debra Toiber and her team at Ben-Gurion University of the Negev believe SIRT6 has “remarkable properties” in regulating mitochondrial function in the brain.
Mitochondria is the energy source cells and many diseases are caused by mutations in the DNA of our mitochondria.
“Mitochondrial dysfunction is one of the hallmarks of aging and one of the main characteristics of multiple neurodegenerative diseases,” said Dr. Toiber.
“Many defects are observed in the mitochondria’s efficiency during aging; however, what initiates these events is unclear.
“We found that SIRT6 keeps mitochondria functioning through the transcription regulation of mitochondrial genes.”
The SIRT6 protein is a key regulator of mitochondrial function in the brain. The decay or absence of it significantly impairs our ability to repair DNA.
“Our results show parallel changes in mitochondrial gene expression induced by the lack of SIRT6 in the brain to the changes observed in aging, Alzheimer’s disease, Parkinson’s disease, and ALS, suggesting that SIRT6 decay in the brain is the driver of these changes,” said Dr. Toiber, who worked alongside teams in the USA and Spain.
Results of their research appear in the peer-reviewed journal Cell Death and Disease.