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Type 2 Diabetes and Obesity Linked to Alzheimer's-Like Neurodegeneration
By Daniel H. Rasolt
Posted: Thursday, September 04, 2008
(Defeat Diabetes® News) -- Type 2 diabetes and obesity, themselves closely linked, have both been shown to hasten the progression of neurodegeneration that strongly parallels Alzheimer's disease (AD), according to a recent study.
Obesity was induced in mice through high fat diets. This had the effect of causing type 2 diabetes with obesity in some mice, and only obesity others, while another non-obese group of mice were used as controls. Brain size and function was then observed in each group.
It was observed that in mice suffering from obesity and type 2 diabetes, brain weight drops, and the ratio of brain weight to body weight is significantly lowered. While certain diminished brain functions associated with AD were observed, it was noted by the authors that obesity and type 2 diabetes did not appear to cause AD, but did expedite its effects. "In essence, the brain shrinks and several biochemical and molecular abnormalities found in patients with AD, including brain insulin resistance, develop with chronic obesity and T2DM [type 2 diabetes mellitus]," says lead researcher Dr. Suzzanne De La Monte. She goes on the say that "the extent of the abnormalities in no way matches AD," indicating that it is not the cause, but more a catalyst for further debilitating effects.
If this study is backed up with evidence from a human model, new philosophies for how to halt the progression of AD should be forthcoming. Firstly, preventing obesity would help prevent the harmful disease diabetes, but managing and preventing both of these conditions, in AD patients that have them, could be essential in preventing the debilitating neurological damage experienced in the progression of AD.
Source: Defeat Diabetes Foundation: De La Monte, Suzzanne. Cawley, Nancy. Journal of Alzheimer's Disease news release. September 2008.
Daniel H. Rasolt writes for Defeat Diabetes® News. Read more of his original content articles.
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