Among neurogenerative diseases, Alzheimer's disease holds a central place. It is responsible for causing dementia—irreversible decline in thinking, memory and ability to perform simple everyday tasks—in 60 to 70 percent of patients. Its causes, sadly, remain poorly understood. However, a new study proposed that the overaction of fructose produced in the brain may be driving the progression of the disease.
Researchers from the University of Colorado Anschutz Medical Campus hypothesized that the disease is propelled mainly by Western culture s led to excessive fructose metabolism in the brain. The study brought together experts across several disciplines, also helped illustrate links such as why obesity and diabetes are linked with higher risks for the 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," said Dr. Richard Johnson, lead author of the study, in a statement.
The role of Fructose
In the study, the researchers drew attention to data that showcased the overactivation of cerebral fructose metabolism which could be driving the disease. The internal or endogenous production in the brain is the primary source of the fructose production the study suggests.
Therefore, the decrease in mitochondrial energy production—generation of energy by the cell organelle mitochondria—is affected by the glycolysis or breakdown of glucose by neurons which is insufficient. This results in a progressive fall in the level of cerebral energy required by the neurons to remain viable and functional.
"By outlining consistent evidence, we're hoping to inspire researchers to continue exploring the relationship between fructose in the brain and Alzheimer's disease. New treatments aimed at inhibiting intracerebral fructose metabolism could provide a novel way to prevent and treat this disease," added Johnson.
Outlining the Metabolism of Fructose
The researchers outlined a scenario that leads to the production of fructose in the study. Here, there is increased oxidative stress (imbalance of antioxidants and free radicals) due to glucose hypometabolism (decreased consumption of glucose), and an accelerating loss of mitochondria. This eventually leads to dysfunctions of the neurons and ultimately death.
In the described scenario, the amyloid plaques (abnormally configured proteins) and neurofibrillary tangles (aggregates of a modified form of a protein known as tau) are components of an inflammatory response and cause injury to the brain.
However, they are not the primary factors driving Alzheimer's disease. According to the authors, in theory, hindering enzymes in the brain that are actively involved in the production of fructose or its metabolism provides novel methods to prevent and treat the disease.