Alzheimer’s disease is one of the most challenging mental health conditions globally and one that scientists and the medical community have not yet figured out. Scientists, however, believe that a better understanding of the underlying mechanism and causes may facilitate the development of a working treatment in the future.
The need to understand more about Alzheimer’s disease has been a key driver for research on the subject. Some researchers believe that the disease might be linked to the overactivation of fructose in the brain. The fructose hypothesis is one that has been championed by researchers from the University of Colorado.
The researchers conducted a study whose findings were published in a journal called the Frontiers in Aging Neuroscience. The research explores the possibility that Alzheimer’s disease might be triggered by too much fructose metabolism in the brain, as a result of heavy western culture influence when it comes to eating habits. The research was a collaborative effort between sugar metabolism experts and neuroscientists. It also attempts to explain the correlation between Alzheimer’s and other conditions, such as obesity and diabetes. The two conditions increase the risks of Alzheimer’s disease.
“In essence, we propose that Alzheimer’s disease is a modern disease driven by changes in dietary lifestyle in which fructose can disrupt cerebral metabolism and neuronal function,” stated Dr. Richard Johnson, who is a medicine professor at the University of Colorado.
The research indicated that there was overactivation of fructose within the cerebral cortex, and it is a major contributor to the onset of Alzheimer’s disease. This excessive production of fructose causes inadequate neuronal glycolysis, which causes a decline in mitochondrial energy production. These events subsequently decrease cerebral energy, which is needed to facilitate neurons’ normal function.
One of the researchers’ observations was that glucose hypometabolism caused more oxidative stress, thus leading to the loss of mitochondria. This mitochondrial loss eventually causes neural dysfunction and the death of neurons. The discoveries might also pave the way for the development of future therapies. For example, it could be used to develop therapies that block the production of enzymes in the brain that facilitate fructose production in the brain.