Geriatric Healthcare Specialist Louisburg NC

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.

Nicole A Collins
(919) 496-4250
205 Sandalwood Ave
Louisburg, NC
Nicole Annette Collins, MD
919-496-4250
PO Box 589
Louisburg, NC
Mary Edith Watkins
(252) 438-2994
Henderson, NC
Jamshed K Khan
(910) 739-7551
395 W 27th St
Lumberton, NC
Pearl Seo
(919) 684-8111
4101 N Roxboro St
Durham, NC
William A Sayles
(919) 496-3680
601 N Bickett Blvd
Louisburg, NC
Farasat Iqbal Ashraf, MD
Zebulon, NC
Hal T Stoneking
(336) 274-3241
301 E Wendover Ave
Greensboro, NC
Kesi Tabia Kindle, MD
252-816-4100
4975 Seward Rd
Pfafftown, NC
DelBert Wayne Ham
(336) 768-3296
190 Kimel Park Dr
Winston-Salem, NC
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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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