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SPORTS MEDICINE :
MEDICAL: CONDITIONS: OBESITY :
MEDICAL: DISEASES: DIABETES :
MEDICAL: DISEASES: ALZHEIMERS :
MEDICAL: RESEARCH :
STUDIES:
Not Just Diabetes and Obesity.
Excess Sugar Intake May Also Cause Alzheimer's Disease
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Not Just Diabetes and Obesity.
Excess Sugar Intake May Also Cause Alzheimer's Disease
Updated: Feb 25, 2017 15:11 IST
Those who consume high sugar diets may be more susceptible to Alzheimers
disease, says a new study.
HEALTH AND FITNESS
Hindustan Times
http://www.hindustantimes.com/health-and-fitness/
not-just-diabetes-and-obesity-excess-sugar-intake-
may-also-cause-alzheimer-s-disease/story-fnqRO0lBC3ZkG5hdw5zyaJ.html
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A shorter URL for the above link:
.
http://tinyurl.com/gokovpb
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ALSO
Henry Bodkin
23 FEBRUARY 2017 11:31AM
The Telegraph
http://www.telegraph.co.uk/science/2017/02/23/
alzheimers-could-caused-excess-sugar-new-study-finds-molecular/
OR
http://tinyurl.com/j27yj8v
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.
People who eat diets high in sugar may be at an increased risk of
Alzheimers disease, a new study has warned.
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For the first time a tipping point molecular link between the blood sugar
glucose and Alzheimers disease has been established by scientists from the
University of Bath and Kings College London in the UK.
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They have shown that excess glucose damages a vital enzyme involved with
inflammation response to the early stages of Alzheimers. Abnormally high
blood sugar levels, or hyperglycaemia, is well-known as a characteristic
of diabetes and obesity, but its link to Alzheimers disease is less
familiar.
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Diabetes patients have an increased risk of developing Alzheimers disease
compared to healthy individuals.
.
snip
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By studying brain samples from people with and without Alzheimers using a
sensitive technique to detect glycation, the team discovered that in the
early stages of Alzheimers glycation damages an enzyme called MIF
(macrophage migration inhibitory factor) which plays a role in immune
response and insulin regulation.
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MIF is involved in the response of brain cells called glia to the build-up
of abnormal proteins in the brain during Alzheimers disease, and the
researchers believe that inhibition and reduction of MIF activity caused
by glycation could be the tipping point in disease progression.
.
It appears that as Alzheimers progresses, glycation of these enzymes
increases.
.
snip
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Normally MIF would be part of the immune response to the build-up of
abnormal proteins in the brain, and we think that because sugar damage
reduces some MIF functions and completely inhibits others that this could
be a tipping point that allows Alzheimers to develop, said van den Elsen.
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The complete article may be read at the URL above.
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Macrophage Migration Inhibitory Factor is subjected to glucose
modification and oxidation in Alzheimers Disease
Omar Kassaar, Marta Pereira Morais, Suying Xu, Emily L. Adam, Rosemary C.
Chamberlain, Bryony Jenkins, Tony James, Paul T. Francis, Stephen Ward,
Robert J. Williams & Jean van den Elsen
Scientific Reports 7, Article number: 42874 (2017)
doi:10.1038/srep42874
GlycobiologyProteomic analysis
Received:
05 August 2016
Accepted:
16 January 2017
Published online:
23 February 2017
Abstract
Glucose and glucose metabolites are able to adversely modify proteins
through a non-enzymatic reaction called glycation, which is associated
with the pathology of Alzheimers Disease (AD) and is a characteristic of
the hyperglycaemia induced by diabetes. However, the precise protein
glycation profile that characterises AD is poorly defined and the
molecular link between hyperglycaemia and AD is unknown. In this study, we
define an early glycation profile of human brain using fluorescent
phenylboronate gel electrophoresis and identify early glycation and
oxidation of macrophage migration inhibitory factor (MIF) in AD brain.
This modification inhibits MIF enzyme activity and ability to stimulate
glial cells. MIF is involved in immune response and insulin regulation,
hyperglycaemia, oxidative stress and glycation are all implicated in AD.
Our study indicates that glucose modified and oxidised MIF could be a
molecular link between hyperglycaemia and the dysregulation of the innate
immune system in AD.
Nature
http://www.nature.com/articles/srep42874
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Temple University
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