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Can the GLUT1 protein Help Alzheimer’s Patients?

Posted by MullanMichael on June 21, 2015

Degenerative GLUT1 protein is a causal factor in neurological degeneration


The GLUT1 protein serves as a driver of glucose across the blood-brain barrier. The blood-brain barrier separates the brain from the circulatory system and protects it from harmful chemicals. It is a highly sophisticated network of dynamic cellular barriers. Glucose, which is vital to the healthy functioning of the body is carried across this blood-brain barrier by GLUT1, a protein whose job it is to ensure a good flow of blood through the brain’s capillaries.

A new study by Keck School of Medicine published recently in “Nature Neuroscience” sought to build on previous research proving that patients exhibiting a higher genetic risk to Alzheimer’s also have low levels of glucose in their systems. This glucose deficiency was found to be due to abnormalities in GLUT1. Researchers found that rather than glucose deficiencies being a result of Alzheimer’s, it was actually the cause of the neurological deterioration so common in Alzheimer’s patients.

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New research study confirms earlier findings


Keck researchers found that when GLUT1 is not at normal levels, glucose movement across the blood-brain barrier is impeded, and cognitive functioning of Alzheimer’s is negatively impacted. This would seem to indicate that if one can manipulate the protein, perhaps there is a chance to retard or stop the progression of neurological decline.

Using a research study pool of mice, Keck School of Medicine researches set out to establish the degree of GLUT1’s role in ensuring a healthy flow of blood in the brain, as well as maintaining the well-being of the blood-brain barrier. The study confirmed that when GLUT1 was at an imperfect level, glucose flow across the blood-brain barrier was reduced. More importantly, after six months of reduced glucose absorption, the mice subjects began to exhibit abnormal behavior patterns, neural dysfunction and neurological degeneration. Additionally, abnormal levels of amyloid-beta were found in their systems.
Researchers have more investigation ahead of them, but thus far the results offer promise for early intervention for Alzheimer’s patients.

 

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