This review is disturbing to me. It seems to imply that even if someone has their weight and blood sugar under control there is a completely different mechanism underlying the "brain diabetes."
I put in italics the part I consider hopeful. IF we can figure out how to slow that down hopefully we can slow down Alzheimer's.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed
The bold and italics text is mine.
Altogether, the results from these studies provide strong evidence in support of the hypothesis that AD represents a form of diabetes mellitus that selectively afflicts the brain. ...The human and experimental animal model studies also showed that CNS impairments in insulin/IGF signaling mechanisms can occur in the absence of T1DM or T2DM. Finally, we demonstrated that although obesity with T2DM causes brain insulin resistance with some features of AD-type neurodegeneration, the effects are relatively modest, not associated with significant histopathological lesions, and lack most of the critical abnormalities that typify AD. Therefore, T2DM was deemed not sufficient to cause AD, although it could possibly serve as a cofactor in its pathogenesis or progression. Altogether, the data provide strong evidence that AD is intrinsically a neuroendocrine disease caused by selective impairments in insulin and IGF signaling mechanisms, including deficiencies in local insulin and IGF production. At the same time, it is essential to recognize that T2DM and T3DM are not solely the end results of insulin/IGF resistance and/or deficiency, because these syndromes are unequivocally accompanied by significant activation of inflammatory mediators, oxidative stress, DNA damage, and mitochondrial dysfunction, which contribute to the degenerative cascade by exacerbating insulin/ IGF resistance. Referring to AD as T3DM is justified, because the fundamental molecular and biochemical abnormalities overlap with T1DM and T2DM rather than mimic the effects of either one.
