Researchers at the Ben-Gurion University of the Negev (BGU) say they have verified the absence of a protein in Alzheimer’s disease patients, and that absence likely contributes to the onset of the debilitating disease.
The common consensus is that aging is the result of DNA damage accumulation — essentially the body’s failure to implement processes to completely repair its DNA.
According to the Alzheimer’s Association, of the estimated 5.5 million Americans living with Alzheimer’s dementia in 2017, 5.3 million are age 65 and older and the remaining 200,000 have younger-onset Alzheimer’s. One in 10 people age 65 and older, 10 percent, has Alzheimer’s dementia.
According to the study, published last month in Cell Reports, one of the key components in this DNA repair process is the protein SIRT6. BGU researchers determined in mouse models that high levels of SIRT6 facilitate DNA repair while low levels enable DNA damage accumulation.
“We analyzed samples from patients with AD and found a remarkable reduction in SIRT6 at both protein and mRNA levels,” they wrote. “Together, our findings indicate that SIRT6 protects the brain from naturally accumulating DNA damage, in turn protecting against neurodegeneration.”
The researchers also tested their hypothesis on neurodegenerative diseases besides Alzheimer’s, and found a deficiency of the SIRT6 protein in patients.
“If a decrease in SIRT6 and lack of DNA repair is the beginning of the chain that ends in neurodegenerative diseases in seniors, then we should be focusing our research on how to maintain production of SIRT6 and avoid the DNA damage that leads to these diseases,” lead author Dr. Deborah Toiber of the BGU Department of Life Sciences said in a statement.
Toiber’s lab is one of only a handful worldwide looking at the effects of SIRT6 in the brain and its connection to neurodegenerative diseases, the statement said.
The study was supported by the Israeli Ministry of Science and Space.