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Published on: February 1, 2017
by Science Daily:
Memory loss and cognitive decline are commonly thought to be the earliest signs of the disorder, but a new study has found declines in glucose levels in the brain come even sooner. Even better? The same team also believes they have figured out a way to stop these levels from falling in the first place, a finding that could potentially prevent Alzheimer’s.
Although doctors have long noted the association between declining glucose levels in the brain and the onset of Alzheimer’s disease, for the first time ever, a study now published online in the journal Translational Psychiatry has proved that these declining energy levels are a direct trigger for the cognitive impairments traditionally associated with the disease. According to a recent statement on the study, this may explain why diabetes, a condition in which glucose cannot enter the cells, is a known risk factor for dementia. According to the study, a protein known as p38 may be able to prevent this deprivation from occurring.
“The findings are very exciting,” explained lead researcher Dr. Domenico Praticò in a statement. “There is now a lot of evidence to suggest that p38 is involved in the development of Alzheimer’s disease.”
For the study, the team purposely deprived the brains of mice of glucose in order to observe the result. As expected, these mice exhibited signs of decline to suggest that neural communication pathways in their brains had broken down. What’s more, the glucose-deprived mice performed significantly worse than control mice in maze memory tests. These mice also displayed high levels of phosphorylated tau and dramatically increased amounts of cell death in the brains, two other well known indications of Alzheimer’s onset.
The study also identified p38 as a possible candidate for the development of a drug to prevent the onset of cognitive decline caused by low glucose levels. According to the research, this protein is naturally made in the body as a response to glucose deprivation. Future research will further investigate p38’s role in memory impairments.
Preventing Alzheimer’s disease is a major goal for scientists around the world, and this year there have been several breakthroughs in this effort. For example, this July a team from Flinders University in Adelaide Australia in partnership with a research team at the Institute of Molecular Medicine, and University of California, Irvine released their efforts on creating a drug that could prevent brain protein buildup, the main hallmark of the disease. According to the research, these findings could lead to a vaccine against Alzheimer’s in as little as five years.
Along the same vein, researchers from Baylor College of Medicine, Texas Children’s Hospital and Johns Hopkins University School of Medicine are hoping to create a pill that when taken could prevent the accumulation of toxic molecules in the brain that eventually go on to form these brain plaques.
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