Look at your notes:Nerve cells die, brain tissue loss it causes brain to be smaller.
This is the transport system of nutrients to the brain, it is held together by a protein (tau). In AD brains this protein doesn’t function properly and causing the tracks to collapse and tangle around each other. Nutrients can’t get to the brain and cells begin to die.
Look at notes:The cause of AD is completely unknown, and therefore there is no cureWith such a significant amount of people with AD researchers are trying to decipher the mysteries of AD.
So how does glucose relate to AD.This got people thinking could low glucose levels be related to Alzheimer’s disease.
In order to determine if there was a relationship between AD and glucose the…
Their studies determined significant variations in the glucose levels of AD patients versus healthy patients which brought them to the conclusion that…
But now how exactly are they relatedLiu and comrades decided to study if the glucose deficiencies in AD brains had something to do with glucose transporters
They have found that AD brains are GLUT1 and GLUT3 deficientAnd they believe this may cause alterations in glucose metabolism.
they were able to conclude that the levels for all four GLUTs were altered differently in the brain. The levels of GLUTs 1 and 3 were significantly reduced in AD brains than in normal healthy brains. Another significant and surprising finding was that GLUT-2 was highly increased in AD brains.
Earlier I had mentioned that tau held together transport system of nutrients to the brain and that in AD brains this protein doesn’t work properlyThe reason is that GLUTs (GLUT 1 and 3) are tied to tau phosphorylation
When glucose metabolism becomes impared it triggers neurodegeneration
This results aren’t certain and more studies must be conducted to fully assert this.
Research should continue to focus on the area of glucose metabolism and ADThe findings made brings science closer to deciphering the cause of AD and in turn closer to finding a cure.
Alzheimer is a progressive brain disease. It is a type of dementia that causes problems with memory, thinking, behavior, and other cognitive functions. It mainly affects those from the ages of sixty to eighty. (ADEAR )
AD brains are significantly smaller than normal brains and they contain disrupted brain tissue. Three main abnormalities:1. amyloid plaques2. neurofibrillary tangles3. loss of connections between neurons and the brain.
Amyloid plaques- abnormal clumps that contain remnants of neurons and other nerve cells. Loss of connection between neurons and the brain.
Neurofibrillary tangles (transport system, held together by tau, collapses and desintigrates)
Stage 1: Mild AD ▪ is mainly characterized by the loss of memory and changes in cognitive functions. Stage 2: Moderate AD ▪ damage of brain areas that control language, reasoning, sensory processing, and conscious thought. Stage 3: Severe AD ▪ almost the entire brain has been affected and the person has reached a vegetative state.
It is estimated that around 5.1 million Americans may have Alzheimer, and by midcentury this figure will reach 16 million. The cause of AD is unknown, and, therefore, no cure has been developed. (ADEAR )
Glucose is the main source of fuel for the brain. Neurons are unable to produce a sufficient amount of glucose and they have a limited supply they can store. The brain’s cognitive functions are highly dependent of a constant, uninterrupted flow of glucose.
Research Glucose metabolism in the region of the hippocampus was examined. All patients were given an oral glucose dosage and were then examined using H MRS to measure glucose concentrations. (Haley et al 2006)
Results: AD Patients Healthy Healthy Elderly Young N 8 14 14 Pre-Glucose 89.96 ± 7.47 82.14 ± 7.25 76.23 ± 4.49 Post-Glucose 139.43±57.81 158.29±30.50 115.08±27.12 The results indicate that the levels of glucose are highly related with Alzheimer’s Disease
Glucose transporters (GLUTS) are vessels that facilitate glucose transport to the brain, since they can go through the blood brain barrier. Currently there are 14 known GLUTS in the human body. Four of them have been found in the brain. (Liu et al,. 2007)
GLUT1 Responsible for transporting glucose from the blood to extracellular space in the brain. GLUT2 Has been identified in brain astrocytes. GLUT3 transports glucose from extracellular space in the brain to neurons GLUT4 Is found inside neurons and it’s is insulin intolerant
AD brains have been found to be GLUT1 and GLUT3 deficient. GLUTs 1-4 were evaluated for alterations in AD brains. Abnormalities in GLUTs 1 and 3 were evaluated to see if they had any effect in glucose metabolism in the brain. (Liu,. 2007)
They concluded that the levels for all four GLUTs were altered differently in the brain. 300 250 200 150 Healthy brains AD brains 100 50 0 GLUT 1 GLUT 2 GLUT 3 GLUT 4
They found that GLUTs 1 and 3 held a significant tie to tau phosphorylation. Tau phosphorylation is important because it is in charge of glucose metabolism regulation.
The decrease in GLUTs 1 and 3 causes tau to become hyperphosphorylated, this causes causing deficiencies and abnormalities in glucose metabolism. Glucose metabolism then becomes impaired, which in turn triggers neurodegeneration.
Knowing that cognitive function is highly dependent on glucose metabolism and adequate glucose levels in the brain, the question of whether artificial sweeteners, such as aspartame, may cause inefficiencies in the necessary amount of glucose to the brain has continuously been brought up.
Determine whether glucose had an effect on memory performance. They had people perform memory tests while being administered glucose before, after, and during each test. (Sünram-Lea et al)
The results showed that there were some significant improvements in the overall scoring of those who were administered the glucose versus the aspartame drink. These findings provide evidence that glucose has a close relation to memory.
These new developments in glucose metabolism and AD are very significant for science, and AD research should continue to focus on this particular area. In regards to AD and artificial sweeteners, research should continue in order to solidly prove if artificial sweeteners do really have an effect on AD.
1. ADEAR.Alzheimer’s Disease: Unraveling the Mystery. [Internet] [http://www.nia.nih.gov/Alzheimers/Publication s/Unraveling/] 2. Haley A.P., Knight-Scott J., Simnad V.I., Manning C.A., 2006. Increased glucose concentration in the hippocampus in early Alzheimer’s disease following oral glucose ingestion. Magnetic Resonance Imaging, 715- 720.
3. Liu Y., Liu F., Iqbal K., Grundke-Iqbal I., Gong C., 2007. Decreased glucose transporters correlate to abnormal hyperphosphorylation of tau in Alzheimer’s disease. FEBS Leters, 359-364. 4. Sünram-Lea S., Foster J.K, Durlach P., Perez C., 2002. The effect of retrograde and terograde glucose administration on memory performance in healthy young adults. Behavioral Brain Reaserch, 505-516.
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