Geriatric Healthcare Specialist Lynnwood WA

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.

Richard Kelsey Tompkins, MD
206-386-9500
15407 14th Dr SE
Mill Creek, WA
Robert Gerard Haining
(206) 365-4222
1570 N 115th St
Seattle, WA
Thomas Edward Phillips
(206) 542-5656
1355 N 205th St
Shoreline, WA
Connie Jo Smith
(425) 899-6800
11521 Ne 128th St
Kirkland, WA
Arthur Calvert Israel
(425) 899-6800
11521 Ne 128th St
Kirkland, WA
Sabine Preyss-Friedman, MD
206-731-5415
10573 14th Ave NW
Seattle, WA
Nargis Naheed, MD
718-270-1432
Seattle, WA
Thomas Edward Phillips, MD
206-542-5656
10734 11th Ave NW
Seattle, WA
Richard Kent Lipsky
(425) 899-6800
11521 Ne 128th St
Kirkland, WA
John C Chen
(206) 522-6047
8659 Inverness Dr Ne
Seattle, WA
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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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