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Patricio Reyes M.D., F.A.N.N.
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Barrow Neurological Institute
St. Joseph's Hospital and Medical Center
"2 NEW THERAPIES FOR ALZHEIMER'S"
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"2 NEW THERAPIES FOR ALZHEIMER'S"
Patricio Reyes M.D., F.A.N.N.
Director, Traumatic Brain Injury, Alzheimer's Disease & Cognitive Disorders Clinics; Phoenix, AZ; Chief Medical Officer, Retired NFL Players Association

St. Joseph's Hospital and Medical Center



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Patricio Reyes M.D.
Director, Traumatic Brain Injury, Alzheimer's Disease & Cognitive Disorders Clinics; Phoenix, AZ; Chief Medical Officer, Retired NFL Players Association

Barrow Neurological Institute

St. Joseph's Hospital and Medical Center
"PRESERVING BRAIN FUNCTIONS "
Runtime: 50:22
Runtime: 50:22
"2 NEW THERAPIES FOR ALZHEIMER'S"
Runtime: 10:27
Runtime: 10:27
ALZHEIMER'S AWARENESS PROGRAMS
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BIOMEDICAL RESEARCH IN ALZHEIMER'S DISEASE
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Robert F. Spetzler M.D.
Director, Barrow Neurological Institute

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Professor Section of Neurosurgery
University of Arizona
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Alzheimer's Disease and Cognitive Disorders Clinic

Barrow Neurological Clinics
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Saturday, February 25, 2017

 

Alzheimer's disease: Molecular study clarifies potential link to high blood sugar





























A new molecular study reveals for the first time that high blood sugar or glucose damages an important enzyme that is involved with how the immune system responds in the early stages of Alzheimer's disease. The researchers say the findings will help map the progression of the devastating disease to better identify those at risk and perhaps find new ways to treat or prevent it.

Abnormally high blood sugar, or hyperglycemia, is a well-known characteristic of diabetes and obesity.

However, apart from the fact that people with diabetes have a higher risk of developing Alzheimer's disease, the link between hyperglycemia and this common cause of dementia has been less clear.

Now, researchers show that macrophage migration inhibitory factor (MIF) - an enzyme that plays an important role in immune function and insulin regulation - undergoes damage associated with high glucose in early Alzheimer's disease.

The team - from the University of Bath and King's College London, both in the United Kingdom - describes the findings in a paper published in the journal Scientific Reports.

Toxic changes in the brain
Alzheimer's is a progressive brain-wasting disease that erodes people's ability to remember, think, perform daily tasks, and lead an independent life.

Among older adults, Alzheimer's disease is the most common cause of dementia, a condition that affects 46 million people worldwide.

As more studies are done, scientists are gradually unraveling the complex changes that happen in the brain during the onset and development of the disease.

Many experts believe the damage caused by Alzheimer's disease starts 10 years or more before the cognitive decline becomes apparent.

During this preclinical stage, when people appear symptom-free, toxic changes are taking place in the brain.

One of the main changes occurring in the brain is the accumulation of abnormal proteins into toxic plaques and tangles, causing once-healthy cells to stop working, lose connections with other cells, and die.

Scientists already knew that glucose and its metabolic byproducts can damage proteins through a reaction called glycation, which has also been linked to Alzheimer's disease, and is a known feature of the hyperglycemia induced by diabetes.

For the new study, the researchers used a sensitive technique to detect glycation in brain samples from people with and without Alzheimer's disease.

Sugar damage to enzyme could be 'tipping point'
The team found evidence that the enzyme MIF undergoes glycation damage in the early stages of the disease. It also seems that the extent of MIF glycation increases as the disease progresses.

MIF is involved in how brain cells called glia respond to the buildup of the abnormal proteins during Alzheimer's disease.

The team suggests that sugar damage to MIF reduces some of the enzyme's functions and blocks others completely, and this could be the "tipping point" that allows Alzheimer's to develop.

"We've shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer's disease," says Jean van den Elsen, one of the senior investigators and professor in biology and biochemistry at Bath.

He and his colleagues are now investigating if they can detect similar changes in the blood.

Story Source: The above story is based on materials provided by MEDICALNEWSTODAY
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