More proof your doctor should have a diet protocol for you. Is this glucose deprivation during the stroke a likely cause of greatly increasing your chance of dementia/Alzheimers post-stroke? WHOM will answer and solve that simple question?
http://www.alzheimersweekly.com/2017/02/more-evidence-alzheimers-is-type-of.html
MEMORY PROBLEMS are an early sign of Alzheimer's. New research directly
links these problems to sugar (glucose) deprivation in brain cells. In
diabetes, a well-known Alzheimer's risk factor, sugar is blocked from
entering cells. How likely does this make the Alzheimer's-sugar-diabetes
triangle?
(Philadelphia, PA) - One of the earliest signs of Alzheimer's disease is
a decline in glucose levels in the brain. It appears in the early
stages of mild cognitive impairment -- before symptoms of memory
problems begin to surface. Whether it is a cause or consequence of
neurological dysfunction has been unclear, but new research at the Lewis
Katz School of Medicine at Temple University now shows unequivocally
that glucose deprivation in the brain triggers the onset of cognitive
decline, memory impairment in particular.
As diabetes is a condition in which glucose cannot enter the cell, this
research gives good reason to suggest that Alzheimer's is caused by a
pathway similar or related to a type of diabetes. This possibility is
strengthened by the fact that insulin resistance in type 2 diabetes is a
known risk factor for dementia.
"In recent years, advances in imaging techniques, especially positron
emission tomography (PET), have allowed researchers to look for subtle
changes in the brains of patients with different degrees of cognitive
impairment," explained Domenico Praticò, MD, Professor in the Center for
Translational Medicine at the Lewis Katz School of Medicine at Temple
University (LKSOM). "One of the changes that has been consistently
reported is a decrease in glucose availability in the hippocampus."
The hippocampus plays a key role in processing and storing memories. It
and other regions of the brain, however, rely exclusively on glucose for
fuel -- without glucose, neurons starve and eventually die.
The new study, published online January 31 in the journal Translational
Psychiatry, is the first to directly link memory impairment to glucose
deprivation in the brain specifically through a mechanism involving the
accumulation of a protein known as phosphorylated tau.
"Phosphorylated tau precipitates and aggregates in the brain, forming
tangles and inducing neuronal death," Dr. Praticò explained. In general,
a greater abundance of neurofibrillary tau tangles is associated with
more severe dementia.
The study also is the first to identify a protein known as p38 as a
potential alternate drug target in the treatment of Alzheimer's disease.
Neurons activate p38 protein in response to glucose deprivation,
possibly as a defensive mechanism. In the long run, however, its
activation increases tau phosphorylation, making the problem worse.
To investigate the impact of glucose deprivation on the brain, Dr.
Praticò's team used a mouse model that recapitulates memory impairments
and tau pathology in Alzheimer's disease. At about 4 or 5 months of age,
some of the animals were treated with 2-deoxyglucose (DG), a compound
that stops glucose from entering and being utilized by cells. The
compound was administered to the mice in a chronic manner, over a period
of several months. The animals were then evaluated for cognitive
function. In a series of maze tests to assess memory, glucose-deprived
mice performed significantly worse than their untreated counterparts.
When examined microscopically, neurons in the brains of DG-treated mice
exhibited abnormal synaptic function, suggesting that neural
communication pathways had broken down. Of particular consequence was a
significant reduction in long-term potentiation- - the mechanism that
strengthens synaptic connections to ensure memory formation and storage.
Upon further examination, the researchers discovered high levels of
phosphorylated tau and dramatically increased amounts of cell death in
the brains of glucose-deprived mice. To find out why, Dr. Praticò turned
to p38, which in earlier work his team had identified as a driver of
tau phosphorylation. In the new study, they found that memory impairment
was directly associated with increased p38 activation.
"The findings are very exciting," Dr. Praticò said. "There is now a lot
of evidence to suggest that p38 is involved in the development of
Alzheimer's disease."
The findings also lend support to the idea that chronically occurring,
small episodes of glucose deprivation are damaging for the brain. "There
is a high likelihood that those types of episodes are related to
diabetes, which is a condition in which glucose cannot enter the cell,"
he explained. "Insulin resistance in type 2 diabetes is a known risk
factor for dementia."
According to Dr. Praticò, the next step is to inhibit p38 to see if
memory impairments can be alleviated, despite glucose deprivation. "It
is an exciting avenue of research. A drug targeting this protein could
bring big benefits for patients," he added.
MORE INFORMATION:
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Other researchers involved in the new study include Elisabetta Lauretti,
Jian-Guo Li, and Antonio Di Meco in the Department of Pharmacology and
Center for Translational Medicine at LKSOM.
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The research was supported in part by a grant from the Wanda Simone Endowment Fund for Neuroscience.
SOURCE:
Temple Health
Hongye Zhao1,2, 
Changkai Sun1,4*
