Insulin has the potential to be developed as a therapeutic agent for Alzheimer's
( a potential rational mechanism )
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A low dose of insulin has been found to suppress the expression in the blood of four precursor proteins involved in the pathogenesis of Alzheimer's disease, according to new clinical research by University at Buffalo endocrinologists. One of the four proteins shown in the study to be suppressed by insulin is a precursor to beta amyloid, the main component of plaques considered the hallmark of Alzheimer's disease.
The findings also demonstrate for the first time that the four precursor proteins studied are expressed in peripheral mononuclear cells, white blood cells that are an important component of the immune system. The low-dose insulin was found to suppress the expression of amyloid precursor protein, from which beta amyloid is derived. It also suppressed presenilin-1 and presenilin-2, the two subunits of an enzyme that converts amyloid precursor protein into beta amyloid, which forms the amyloid plaques. Insulin also suppressed glycogen synthase kinase, which phosphorylates, or adds on another phosphate group, to another neuronal protein, tau, to form the neurofibrillary tangles, the other important component of Alzheimer's disease in the brain. Read more: sciencedaily.com
Nutrigenomics could provide nutrition relevant biomarkers
The benefits of nutrigenomics tools to illuminate the effect of certain nutrients on genes are occurring right now, but talk of personalized nutrition should be left for the future, says a DSM corporate scientist. Read more: nutraingredients.com
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