Scientists Discover How Too Much Sugar Intake May Raise Alzheimer’s Risk

Sugar Intake May Raise Alzheimer’s Risk

The precise biological mechanisms underlying this association between high blood sugar levels and an elevated risk of Alzheimer’s were previously unknown. A recent investigation into ATP-sensitive potassium (KATP) channels, which control cellular activity based on energy levels, has now clarified the relationship. It opens the door for potential novel therapies focused on particular channels as a fresh approach to treating the condition.

Although it is well known that patients with type 2 diabetes have a higher chance of getting Alzheimer’s, the precise explanation for this is still unclear and is the subject of ongoing research.

Recent research from Wake Forest University School of Medicine published in JCI Insight has revealed a novel mechanism that raises the risk of Alzheimer’s. According to the study, elevated blood glucose levels and higher sugar consumption are sufficient to produce amyloid plaque formation in the brain.

The study gives significant insights into the metabolic abnormalities linked with diabetes that make the brain vulnerable to Alzheimer’s.

Sugar linked to the development of toxic Alzheimer’s plaques

The study concentrated on a particular class of channels known as ATP-sensitive potassium (KATP) channels, which are crucial in controlling cell activity according to energy levels. The neuronal circuitry of the brain has a significant expression of KATP channels.

The researchers used a mouse model to show that consuming sugar water rather than regular drinking water increases the production of amyloid plaques.

Additionally, they found that higher blood sugar levels influence the brain’s beta-amyloid synthesis.

These results support the hypothesis that blood glucose levels and sugar consumption directly impact amyloid plaque generation, a significant hallmark of Alzheimer’s.

What are the cellular mechanisms underlying sugar’s influence on the brain?

The research team discovered a class of metabolic sensors termed ATP-sensitive potassium channels, or KATP channels, found in neurons while examining the underlying mechanisms. These pathways link changes in metabolism, neuronal activity, and beta-amyloid synthesis in the brain.

These KATP channels serve as energy regulators by monitoring the availability of ATP. ATP (Adenosine Triphosphate) is a vital energy source for cellular survival.

Disrupting the normal function of these sensors can disturb the brain’s regular functions and have consequences on its general functionality.

The researchers observed the expression of these metabolic sensors in Alzheimer’s patient’s brains. They again noticed changes in the presence of these channels.

According to the principal investigator, Dr. Shannon Macauley, they eliminated these sensors from the brain of mice using genetic procedures, demonstrating that a rise in blood sugar did not lead to an increase in beta-amyloid levels or amyloid plaques. The expression of these channels varies with an Alzheimer’s diagnosis, which again suggests that these metabolic sensors may contribute to the development of Alzheimer’s, as they discovered when they investigated the expression of these metabolic sensors in post-mortem human brains from Alzheimer’s patients.

What possible effects might this have on people who have Alzheimer’s?

This study emphasizes the critical role of KATP channels in the relationship between hyperglycemia and the risk of Alzheimer’s.

Dr. Macauley points out that the study not only provides one theory for why people with type 2 diabetes have an elevated chance of developing Alzheimer’s but also identifies a potential therapeutic target for curing the condition.

According to Dr. Merill, a geriatric psychiatrist and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center in Santa Monica, CA, treatments aimed at clearing up the mess of plaques left behind after the synapses and neurons have already died and gone may be less effective than early detection and correction of underlying drivers of Alzheimer’s, such as an inadequate elevation of blood sugar levels and the associated insulin resistance.

In theory, by targeting the KATP channels, the medications could lessen the influence of hyperglycemia on the formation of beta-amyloid, which is directly associated with the risk of developing Alzheimer’s.


  1. Grizzanti, J., Moritz, W.R., Pait, M.C., Stanley, M., Kaye, S.D., Carroll, C.M., Constantino, N.J., Deitelzweig, L.J., Snipes, J.A., Kellar, D. and Caesar, E.E., 2023. K ATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer’s disease–related pathology. JCI insight, 8(10).
  2. Cross, P.I., Could sugar consumption impact the risk of Alzheimer’s disease? Medical News Today. Published Online: 30th May, 2023. Accessed: 23rd June, 2023.
  3. Scientists discover that metabolic sensor may play role in Alzheimer’s disease. Medical Xpress. Published Online: 22nd May, 2023. Accessed: 23rd June, 2023.
  4. Sweet Trouble: How Sugar Intake Might Increase Alzheimer’s Risk. Published Online: 22nd May, 2023. Accessed: 23rd June, 2023.
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