Scientists reveal link between sugar intake and brain disease
While dementia is a general term for a decline in mental ability severe enough to interfere with one’s daily life, Alzheimer’s is the most common cause of dementia.
What you need to know:
- The study provides valuable insights into the metabolic changes that put individuals with Type 2 diabetes at a higher risk of developing Alzheimer's disease.
- As the prevalence of both diabetes and Alzheimer’s disease continues to rise globally, the discovery of this new pathway offers a potential avenue for intervention and prevention.
Researchers have discovered a mechanism linking increased sugar consumption to the development of Alzheimer's disease. The study published in the journal JCI Insight provides valuable insights into the metabolic changes that put individuals with Type 2 diabetes at a higher risk of developing this debilitating neurological disorder.
Dr Shannon Macauley, the principal investigator of the study and associate professor of physiology and pharmacology at Wake Forest University School of Medicine, explained the significance of their findings. "We wanted a better understanding of the metabolic changes in diabetes that puts the brain at risk for Alzheimer's disease or accelerates the pathology already forming in the brain of individuals who will go on to an Alzheimer's disease diagnosis," she said. Using a mouse model, the research team discovered that consuming sugar water instead of regular drinking water led to an increase in the formation of amyloid plaques, which are composed of toxic proteins in the brain.
Furthermore, elevated blood sugar levels were found to stimulate the production of amyloid-beta, a protein associated with Alzheimer's disease.
"This finding is significant because it demonstrates that consuming too much sugar is enough to cause amyloid plaque proliferation and increase the risk of Alzheimer's disease," stated Dr. Macauley.
To delve deeper into the underlying mechanisms, the scientists identified a group of metabolic sensors called ATP-sensitive potassium (KATP) channels, which play a crucial role in connecting changes in metabolism with neuronal firing and amyloid-beta production. Disrupting these sensors altered the normal functioning of the brain.
The team then explored the expression of these metabolic sensors in the brains of individuals with Alzheimer’s disease. They discovered that the expression of these channels changed in correlation with the presence of Alzheimer’s pathology.
Dr Macauley believes that these metabolic sensors may be key players in the development of Alzheimer’s disease and could potentially pave the way for new treatments. “What’s most notable is that pharmacological manipulation of these KATP channels may hold a therapeutic benefit in reducing amyloid-beta pathology for diabetic and prediabetic patients,” she added.
The study sheds light on the mechanistic link between Type 2 diabetes and Alzheimer’s disease, suggesting that elevated blood glucose levels contribute to increased brain excitability and the release of amyloid-beta.
While further research is needed to fully understand the intricacies of this mechanism, these findings provide hope for the development of targeted therapies aimed at reducing amyloid-beta pathology in individuals with diabetes or prediabetes. As the prevalence of both diabetes and Alzheimer's disease continues to rise globally, the discovery of this new pathway offers a potential avenue for intervention and prevention.The scientific community eagerly awaits further developments in this promising field of research.
