As per the new study data, Scientists has found connections between abnormalities with how the brain breaks down glucose and Alzheimer’s disease pathology and symptoms. National Institute on Aging (NIA) part of the National Institutes of Health has supported this study and appears in the journal Alzheimer’s & Dementia in Nov. 6, 2017.
Investigator and chief of the Unit of Clinical and Translational Neuroscience in the National Institute on Aging’s (NIA) Laboratory of Behavioral Neuroscience- MadhavThambisetty, M.D., Ph.D., conducted a study from participants in the Baltimore Longitudinal Study of Aging (BLSA), it is one of the world’s longest-running scientific studies of human aging researchers looked at brain tissue samples at autopsy,. Over several decades, BLSA tracks psychological, physical, and neurological data on participants.
In different brain regions, researchers have measured the brain glucose levels it was found some susceptible to Alzheimer’s disease pathology, such as temporal cortex and frontal, and it is found some that are resistant like the cerebellum. Three groups of (BLSA) participants during life in the brain at death has analyzed with Alzheimer’s symptoms with Alzheimer’s disease pathology (neurofibrillary tangles and beta-amyloid protein plaques). In the brain post-mortem, it is found that individuals without symptoms during life but with significant levels of Alzheimer’s pathology.
The important process by which the brain breaks down glucose, with evidence linked to the severity of the abnormalities of Alzheimer’s pathology, in glycolysis they found distinct abnormalities. More severe plaques and tangles found in the brains correlates with the lower rates of glycolysis and higher brain glucose levels. Severe reductions in the brain relate to the expression of symptoms of Alzheimer’s disease during life, such as problems with memory.
“Richard J. Hodes, M.D. NIA Director said, Researchers have thought for some time about the possible links between how the Alzheimer’s and brain processes glucose. For better and more effective ways to treat or prevent Alzheimer’s disease research such as this involves new thinking about how to investigate these connections in the intensifying search.”
The similarities between diabetes and Alzheimer’s, is difficult to evaluate. To enter the brain or to get into neurons insulin is not needed for glucose. The researchers by measuring ratios of the amino acids serine, glycine and alanine to glucose examined the brain’s use of glucose. This allowed them to assess the rates of key steps for glycolysis.
After that, they used proteomics the large-scale measurement of cellular proteins to tally the levels of GLUT3, in neurons-a glucose transporter protein. They found that in brains with Alzheimer’s pathology compared to normal brains that GLUT3 levels were lower, and that these levels were also connected to the severity of plaques and tangles, in study participant’s years before they died the team checked blood glucose levels, found that at death, greater increases in blood glucose levels correlated with greater brain glucose levels. “Thambisetty said these findings point in the development of new treatments to a novel mechanism that can be targets to help the brain to overcome glycolysis defects in Alzheimer’s disease”. As of now it is not clearedcompletely whether deformities in other metabolic pathways linked to glycolysis to determine how they may relate to Alzheimer’s pathology in the brain. Further study based on this by Thambisetty and his team.