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A Connection Between Brain Glucose and Alzheimer?

Researchers may have found a connection between the way a patient’s brain breaks down glucose and the risk of developing Alzheimer disease.


 

For some time, researchers have suspected that diabetes and Alzheimer disease (AD) are similar, but those similarities have been hard to evaluate. Insulin is not needed for glucose to enter the brain or to get into neurons. But NIH researchers may have, for the first time, uncovered a connection.

Using brain tissue samples from participants in the Baltimore Longitudinal Study of Aging, one of the longest-running aging studies, the researchers measured glucose levels in different brain regions, including those either vulnerable or resistant to AD.

The researchers found distinct abnormalities in the way the brain breaks down glucose, and say severity of the abnormalities correlated with the severity of AD pathology. Lower rates of glycolysis and higher brain glucose levels correlated to more severe plaques and tangles in the brains of patients with AD. More severe reductions in brain glycolysis also were related to symptoms of the disease during life, such as memory problems.

The researchers caution that it is not yet clear whether abnormalities in brain glucose metabolism are definitively linked to the severity of AD symptoms or the speed of disease progression. However, lead investigator Madhav Thambisetty, MD, PhD, says “these findings point to a novel mechanism that could be targeted in the development of new treatments.”

For some time, researchers have suspected that diabetes and Alzheimer disease (AD) are similar, but those similarities have been hard to evaluate. Insulin is not needed for glucose to enter the brain or to get into neurons. But NIH researchers may have, for the first time, uncovered a connection.

Using brain tissue samples from participants in the Baltimore Longitudinal Study of Aging, one of the longest-running aging studies, the researchers measured glucose levels in different brain regions, including those either vulnerable or resistant to AD.

The researchers found distinct abnormalities in the way the brain breaks down glucose, and say severity of the abnormalities correlated with the severity of AD pathology. Lower rates of glycolysis and higher brain glucose levels correlated to more severe plaques and tangles in the brains of patients with AD. More severe reductions in brain glycolysis also were related to symptoms of the disease during life, such as memory problems.

The researchers caution that it is not yet clear whether abnormalities in brain glucose metabolism are definitively linked to the severity of AD symptoms or the speed of disease progression. However, lead investigator Madhav Thambisetty, MD, PhD, says “these findings point to a novel mechanism that could be targeted in the development of new treatments.”

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