Overeating accelerates the aging of the brain, while restricting food activates a molecule that can help keep it youthful, according to a study published in the Proceedings of the National Academy of Sciences.
As the authors of the study reminded, many studies to date have suggested that overeating and related metabolic diseases (including obesity and type 2 diabetes) adversely affect the brain – they slow down its functioning, accelerate aging, increase susceptibility to brain degenerative diseases typical of old age such as Alzheimer’s or Parkinson’s disease. On the other hand, limiting the caloric content of the diet helps to slow down the aging processes of the body, including the brain, and reduce the death of neurons. However, the precise mechanism responsible for this at the molecular level is not well understood.
Scientists from the Catholic University of the Sacred Heart in Rome, in collaboration with colleagues from Germany, Canada and the United Kingdom, have now shown in experiments on mice that a protein called CREB1 is responsible for the beneficial effects of a less caloric diet on the brain. They are included in the so-called transcription factors that regulate the activity of other genes by binding to DNA. CREB1 activates, among others genes that affect longevity and the proper functioning of the brain in terms of memory, learning and control of anxiety reactions.
Dr. Giovambattista, who leads the research, hopes that in the future it will be possible to find a way to activate CREB1, for example through new drugs, so that the brain can be kept young without the need for a restrictive diet.
The researcher and his colleagues compared the consequences of caloric restriction in the diet of modified mice that did not produce CREB1 protein and their unchanged peers. For five weeks, the animals were either allowed to eat freely or switched to a 30 percent less caloric diet.
This change in nutrition extends the lives of rodents and other animals, according to previous research. Mice on a less nutritious diet do not become obese, do not develop diabetes, and are more cognitively efficient and remember better and are less aggressive. In addition, they do not develop Alzheimer’s disease – or it happens much later than in overfed rodents – and the symptoms are milder.
Interestingly, the effect of restricting food on body weight was similar in both groups of mice. But while the less caloric diet improved memory capacity in unmodified mice, it did not cause similar changes in mice that did not produce CREB1. These rodents performed worse on memory tests than their unchanged peers.
“Our research allowed for the first time to identify the protein responsible for the influence of diet on the brain” – comments Dr. Pani.
The researcher and colleagues also proved that reducing the amount of food does not affect the total level of CREB1 protein, but increases its activity in the cerebral cortex and hippocampus, the structure regulating, among others, memory processes.
Activation of the CREB1 protein, in turn, enhances the production of another protein related to longevity, i.e. sirtuin-1 and proteins that determine the survival of neurons, their plasticity and resistance to stress.
“This discovery could make an important contribution to the design of future therapies to keep the brain young, preventing degeneration and aging. In addition, it sheds light on the relationship between metabolic diseases, such as obesity and diabetes, and a decline in mental performance “- concludes Dr. Pani.