. Cyclohexanehexol inhibitors of Abeta aggregation prevent and reverse Alzheimer phenotype in a mouse model. Nat Med. 2006 Jul;12(7):801-8. PubMed.

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  1. Scyllo-inositol may limit or reverse Alzheimer disease because it appears to inhibit the uptake of myo-inositol in the brain and thus stops the overproduction of D-myo-inositol-1,4,5-triphosphate, a compound which plays a critical role in regulating calcium in the cytoplasm of nerve cells. If there is too much D-myo-inositol-1,4,5-triphosphate, calcium levels should rise. The enzyme which cleaves off the beta amyloid protein may be activated by high intracellular calcium levels. Thus, high levels of D-myo-inositol-1,4,5-triphosphate would likely lead to the aggregation of beta amyloid proteins.

    The high levels of myo-inositol in the pre-dementia phase of people with Down syndrome, and the high levels of myo-inositol monophosphatase (which converts myo-inositol monophosphates into myo-inositol) in post-mortem Alzheimer disease brains implicate myo-inositol in these two forms of dementia. High levels of myo-inositol also correlate with insulin-resistant diabetes, which may help explain the link between diabetes and Alzheimer disease as well as why insulin-like nerve growth factors also show promise against the disease. Myo-inositol monophosphate is produced from glucose-6-phosphate with the phosphate being added by ATP (when glucose enters into a cell it is converted into glucose-6-phosphate; the more glucose that enters into a cell the more glucose-6-phosphate is produced). ATP also probably plays an important role in the conversion process from there: myo-inositol/myo-inositol monophosphate, phosphatidyl-myo-inositol-4,5-biphosphate, myo-inositol-1,4,5-triphosphate. It is possible, however, that phosphates from other sources (phosphoric acids, aluminum phosphates, and biphosphates such as Fosamax) and phosphate analogs (such as aluminum fluoride and sodium fluoride) accelerate the creation of myo-inositol triphosphate and thus the onset of Alzheimer disease.

    Scyllo-inositol may not be as easily taken up into lipids as myo-inositol. "Scyllo-inositol biphosphate" may not be as easy to cleave off from lipids as myo-inositol biphosphates, or "scyllo-inositol triphosphate" may not work with calcium receptors as effectively as myo-inositol triphosphates. The end result should be lower levels of calcium and fewer beta amyloid proteins being generated. The slowing down in the processing of beta amyloid proteins may allow for some or all of those proteins to be moved out of the nerve cells or otherwise eliminated.