Fructose Made in the Brain Could Be a Mechanism Driving Alzheimer’s

Summary: Alzheimer’s disease may be driven by excessive fructose metabolism in the brain. The findings shed light on why diseases, such as diabetes and obesity, are linked to an increased risk of Alzheimer’s.

Source: University of Colorado Anschutz Medical Campus

New research released from the University of Colorado Anschutz Medical Campus proposes that Alzheimer’s disease may be driven by the overactivation of fructose made in the brain.

The study was published in the Frontiers in Aging Neuroscience and outlined the hypothesis that Alzheimer’s disease is driven largely by Western culture that has resulted in excessive fructose metabolism in the brain.

The paper brought together an interdisciplinary team of neurologists, neuorscientists and experts on sugar metabolism, and presents evidence from extensive data and research conducted in Alzheimer’s disease that links high fructose levels in the brain to the disease. It also helps explain associations, such as why diabetes and obesity are associated with an increased risk for 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,” said author Richard Johnson, MD, professor at the University of Colorado School of Medicine on the CU Anschutz Medical Campus.

Johnson outlines data that showcases the overactivation of cerebral fructose metabolism that can drive Alzheimer’s disease. The source of fructose is largely from endogenous production in the brain. Thus, the reduction in mitochondrial energy production is hampered by neuronal glycolysis that is inadequate, resulting in progressive loss of cerebral energy levels required for neurons to remain functional and viable.

This shows an old woman
Johnson outlines data that showcases the overactivation of cerebral fructose metabolism that can drive Alzheimer’s disease. Image is in the public domain.

“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,” Johnson adds.

In one of the scenarios outlined by Johnson and his collaborators, glucose hypometabolism increased oxidative stress, and a progressive loss of mitochondria occured, leading eventually to neuronal dysfunction and death. In this scenario, the amyloid plaques and neurofibrillary tangles are part of the inflammatory response and participate in injury, but are not the central factors driving the disease.

Johnson mentions that theoretically, inhibiting enzymes in the brain that are involved in fructose production or metabolism might provide novel ways to prevent and treat Alzheimer’s disease.

About this Alzheimer’s disease research article

Source:
University of Colorado Anschutz Medical Campus
Contacts:
Julia Milzer – University of Colorado Anschutz Medical Campus
Image Source:
The image is in the public domain.

Original Research: Open access
“Cerebral Fructose Metabolism as a Potential Mechanism Driving Alzheimer’s Disease” by Richard Johnson el al. Frontiers in Aging Neuroscience.


Abstract

Cerebral Fructose Metabolism as a Potential Mechanism Driving Alzheimer’s Disease

The loss of cognitive function in Alzheimer’s disease is pathologically linked with neurofibrillary tangles, amyloid deposition, and loss of neuronal communication. Cerebral insulin resistance and mitochondrial dysfunction have emerged as important contributors to pathogenesis supporting our hypothesis that cerebral fructose metabolism is a key initiating pathway for Alzheimer’s disease. Fructose is unique among nutrients because it activates a survival pathway to protect animals from starvation by lowering energy in cells in association with adenosine monophosphate degradation to uric acid. The fall in energy from fructose metabolism stimulates foraging and food intake while reducing energy and oxygen needs by decreasing mitochondrial function, stimulating glycolysis, and inducing insulin resistance. When fructose metabolism is overactivated systemically, such as from excessive fructose intake, this can lead to obesity and diabetes. Herein, we present evidence that Alzheimer’s disease may be driven by overactivation of cerebral fructose metabolism, in which the source of fructose is largely from endogenous production in the brain. Thus, the reduction in mitochondrial energy production is hampered by neuronal glycolysis that is inadequate, resulting in progressive loss of cerebral energy levels required for neurons to remain functional and viable. 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. Inhibition of intracerebral fructose metabolism could provide a novel way to prevent and treat this disease.

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