A brain protein called Glut1 is often associated with Alzheimer's disease, but has now been found in young brains. The substance is responsible for carrying glucose across the blood-brain barrier that helps to protect the organ.
Alzheimer's patients often show a shortage of the Glut1 protein.
University of Southern California researchers in the Keck School of Medicine believe a shortage of this protein could not only indicate the presence of the disease, but may actually aggravate symptoms.
"We do not know yet whether medicine can restore Glut1 expression, but we believe that targeting the protein may help prevent Alzheimer's from getting worse among individuals predisposed to develop the disease," Berislav V. Zlokovic, director of the Zilkha Neurogenetic Institute at the Keck School of Medicine, said.
Human brains use glucose as their main energy source, and Glut1 carries the chemical over the protective blood-brain layer. This protective barrier normally prevents pathogens in the blood from entering brain tissue. Studies have shown a reduction in glucose uptake among people with a genetic disposition to the disease, as well as those who have the disease, but do not show symptoms.
Alzheimer's disease is the most common form of dementia, affecting around 5.2 million Americans. Symptoms include memory loss, odd behavior, and reduction in a range of mental abilities. Medical researchers believe that up to 16 million people in the United States could suffer from the disease by the middle of the century.
Mice with Glut1 deficiencies were examined as part of the study, and low concentrations of the protein were found to reduce the uptake of glucose by the brain, and result in behavioral changes in the rodents. Brains also started to degenerate, and the blood-brain barrier was reduced in rats as young as six months old. Alzheimer's disease is believed to be fueled by increasing concentrations of amyloid-beta peptides in brains, which results from a breakdown in the barrier.
Some researchers believe these plaques destroy brain neurons, resulting in symptoms, including memory loss, often associated with the disease. Concentrations of these peptides appear to have a genetic correlation, although the nature of that influence remains unknown. Other investigators believe the protein is a byproduct of the disease, which is driven by other factors.
Future research will seek to discover how Glut1 deficiencies affect brain metabolism, and whether changes differ between individuals who experience shortages of the protein early in life, compared to later drops in Glut1 levels.
Analysis of the role of Glut1 in the development of Alzheimer's disease was detailed in the journal Nature Neuroscience.
Photo: Susumu Komatsu | Flickr
