The accumulating evidence that reduced glucose utilization and deficient energy metabolism occur early in the course of disease, suggests a role for impaired insulin signaling in the pathogenesis of Alzheimer disease.

Researchers from Brown University demonstrated che extensive abnormalities in insulin and insulin-like growth factor, types I and II ( IGF-I and IGF-II ) signaling mechanisms in brains with Alzheimer disease, and shows that while each of the corresponding growth factors is normally made in central nervous system ( CNS ) neurons, the expression levels are markedly reduced in AD.

The strikingly reduced CNS expression of genes encoding insulin, IGF-I, and IGF-II, as well as the insulin and IGF-I receptors, suggests that AD may represent a neuroendocrine disorder that resembles, yet is distinct from diabetes mellitus. Therefore, we propose the term, “Type 3 Diabetes” to reflect this newly identified pathogenic mechanism of neurodegeneration.

Source: Journal of Alzheimer’s Disease, 2005

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