Geriatric Healthcare Specialist Mount Pleasant SC

In a study recently published in the Journal of Alzheimer’s Disease, researchers from Brown Medical School found that reduced glucose uptake and decreased metabolism in the hippocampus—the area of the brain associated with memory—cause neurodegeneration and cognitive impairment.

Karleen M McNeal, MD
843-856-0734
1500 Carolina Jasmine Rd
Mt Pleasant, SC
Thomas Bernard Cruden, MD
828-758-1177
1049B Anna Knapp Blvd
Mount Pleasant, SC
Hans Leighton Hinson
(843) 577-5011
109 Bee St
Charleston, SC
Karleen Marie McNeal
(843) 792-1414
171 Ashley Ave
Charleston, SC
John Edgar Kleckley
(843) 965-8265
125 Doughty St
Charleston, SC
Rex Shad Morgan
(843) 388-0106
1230 Hospital Dr.
Mt. Pleasant, SC
Jan Neil Basile
(843) 789-6680
109 Bee St
Charleston, SC
Jerome Edward Kurent, MD
843-792-4554
Rm 1241S Rutledge Towers
Charleston, SC
General T Little, MD
843-722-6336
280 Rutledge Ave
Charleston, SC
Hans Leighton Hinson, MD
312-942-5000
Charleston, SC
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Food for Thought

By Kris Kucera

Rarely does an extended family get a free pass from Alzheimer’s disease or diabetes mellitus. On the surface, these two afflictions appear totally unrelated —Alzheimer’s (AD), Mother Nature’s cruel version of identity theft; and diabetes, the glucose-metabolism disorder that affects both young and old alike. However, new research indicates that the two diseases behave in a similar manner.

In a study recently published in the Journal of Alzheimer’s Disease, researchers from Brown Medical School found that reduced glucose uptake and decreased metabolism in the hippocampus—the area of the brain associated with memory—cause neurodegeneration and cognitive impairment. This, they say, suggests that a form of diabetes, tentatively dubbed type 3, leads to AD.

Type 1 diabetes results from a severe or complete lack of insulin, a hormone made in the pancreas that controls blood sugar. Type 2, dubbed adult onset diabetes (although these days it occurs in teenagers and even younger kids), also stems from a dearth of insulin, or insulin resistance —the existing insulin molecules cannot deliver glucose through the cells’ membranes. Surprisingly, the researchers found a new form of insulin, produced in the brain, and they believe that, over time, decreasing levels of this “brain insulin” and other insulin-related proteins ultimately precipitate AD. While levels of brain insulin have no known affect on a body’s overall blood sugar, scientists have long recognized that diabetes patients are more likely to develop AD than those without the disease.

Skeptics of the Brown team’s findings argue that our brains produce so little insulin in the first place, reduced levels of the hormone can’t possibly play a significant role in AD. Regardless, the new data show that AD may be a neuroendocrine disorder, thus increasing the possibility for more effective treatments. And that gives hope to all of us who may one day be touched, directly or indirectly, by the merciless hand of AD.

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