A protein dubbed SIRT6 is almost completely absent in Alzheimer’s disease patients and this deficiency likely contributes to its onset, according to an Israeli study.

Using mouse models, Ben-Gurion University of the Negev researchers determined that SIRT6 is a key component in the DNA repair process, while low levels of SIRT6 enable DNA damage accumulation.

The body’s failure to implement processes to repair accumulated DNA damage is widely thought to be the cause of conditions associated with aging, such as Alzheimer’s disease.

Writing about their findings in Cell Reports, the researchers also report that a deficiency of the SIRT6 protein was present in neurodegenerative diseases other than Alzheimer’s as well.

“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,” concluded lead author Deborah Toiber of the BGU Department of Life Sciences.

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.

Alzheimer’s Association statistics show an estimated 5.5 million Americans are living with Alzheimer’s dementia in 2017, 5.3 million of whom are age 65 and older.

The study, supported by the Israeli Ministry of Science and Space, also had input from other researchers at BGU and from scientists at Massachusetts General Hospital Cancer Center and its Center for Regenerative Medicine and from the Paul Flechsig Institute for Brain Research at the University of Leipzig.