2. 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 )
3. AD brains are
significantly smaller than
normal brains and they
contain disrupted brain
tissue.
Three main
abnormalities:
1. amyloid plaques
2. neurofibrillary tangles
3. loss of connections
between neurons and
the brain.
4. Amyloid plaques-
abnormal clumps
that contain
remnants of
neurons and other
nerve cells.
Loss of connection
between neurons
and the brain.
5. Neurofibrillary tangles (transport system,
held together by tau, collapses and
desintigrates)
6. 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.
7. 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 )
8. 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.
9. 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)
10. 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
11. 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)
12.
13. 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
14. 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)
15. 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
16. 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.
17. 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.
18. 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.
19. 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)
20. 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.
21. 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.
22. 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.
23. 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.
Notas del editor
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.
