Brain aging can be delayed in mice if they are placed on a high-fat diet, according to a study conducted by the Center for Healthy Aging at the University of Copenhagen in Denmark and the National Institute of Health.
It is normal for defects to appear in the nervous system as people age. Among these, the brain loses some of its intellectual capacity, and the risk of Parkinson’s and Alzheimer’s disease increases.
Although human cells have a system for repairing damage to DNA, this repair function breaks down as we age.
This damage to DNA has been linked with Alzheimer’s and Cockayne syndrome – a premature aging disorder that results in death by the age of 10-12.
The new study uses a mouse model of Cockayne syndrome to investigate these defects to the DNA repair system.
Lead author Prof. Vilhelm Bohr – from the Center for Healthy Aging, University of Copenhagen and the National Institute of Health – describes the team’s findings:
“The study is good news for children with Cockayne syndrome, because we do not currently have an effective treatment. Our study suggests that a high-fat diet can postpone [the] aging processes.”
“A diet high in fat also seems to postpone the aging of the brain. The findings, therefore, potentially imply that patients with Alzheimer’s and Parkinson’s disease in the long term may benefit from the new knowledge,” he adds.
- Symptoms of Cockayne syndrome include dwarfism, mental retardation and hearing and vision impairments
- Cockayne syndrome is linked to a defect in the CSB protein – the main component of the DNA repair system
- Without functioning CBS, protein synthesis fails in cells, which has been described as “the most dramatic of imaginable consequences for an organism.”
The researchers explain that sugar and “ketones” are sources of energy that our brains require a constant supply of. When blood sugar is low, ketones are produced by the body breaking down fat.
The researchers found that the mice with Cockayne syndrome benefited from having an extra supply of similar brain fuel, provided here in the form of medium-chain fatty acids from coconut oil.
Although the researchers did not provide Medical News Today with data on the extent of the improvement in the mice with Cockayne syndrome, Morten Scheibye-Knudsen, from the National Institute of Health, further explains the results.
“In cells from children with Cockayne syndrome,” he says, “we have previously demonstrated that aging is a result of the cell repair mechanism being constantly active.”
“It eats into the resources and causes the cell to age very quickly,” Scheibye-Knudsen adds. “We therefore hope that a diet with a high content of coconut oil or similar fats will have a beneficial effect, because the brain cells are given extra fuel and thus the strength to repair the damage.”