Weekend – October 21-22, 2008

Weekend – October 21-22, 2008

Some of the most important nutrition seminar take-aways: Jelly Bellies equal burpees, and the importance of fire safety on cheat days.

Here is an abstract from a recent study that explores the link between diabetes (impaired insulin response) and Alzheimer’s: Therapeutic Rescue of Neurodegeneration in Experimental Type 3 Diabetes: Relevance to Alzheimer’s Disease. de la Monte SM, Tong M, Lester-Coll N, Plater M Jr, Wands JR, Department of Medicine, Rhode Island Hospital and Brown Medical School, Providence, RI. Journal of Alzheimer’s Disease. 10(1):89-109, 2006 Sep. Alzheimer’s disease (AD) is associated with major impairments in insulin and insulin-like growth factor (IGF) gene expression and signaling in the brain. These abnormalities increase with severity of dementia, and are associated with deficiencies in energy metabolism and acetylcholine homeostasis. The co-existence of brain insulin/IGF deficiency and resistance suggests that AD may represent a brain-specific form of diabetes, i.e. Typediabetes. This hypothesis is supported by the findings in an experimental animal model in which intracerebral (ic) Streptozotocin (STZ) was used to deplete brain and not pancreatic insulin. The ic-STZ treatment produced brain-specific insulin depletion and insulin resistance are associated with progressive neurodegeneration that shares many features in common with AD. We now demonstrate that early treatment with peroxisome-proliferator activated receptor agonists can effectively prevent ic-STZ-induced neurodegeneration and its associated deficits in learning and memory. These effects were mediated by increased binding to insulin receptors, reduced levels of oxidative stress and tau phosphorylation, and increased choline acetyltransferase expression in the brain, suggesting that insulin sensitizer agents may have therapeutic efficacy in early AD.

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