All considered, these data strongly suggest that SAMe depletion contributes to multiple pathophysiological processes observed in the AD brain, including the unsilencing of genes involved in AD development and progression, the depletion of acetylcholine, and the inability to appropriately dephosphorylate tau
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The phosphatidyl inositol kinases (PIK3, PIK4, PIK5) directly phosphorylate PI to yield mono, di and tri-phosphorylated-phosphoinositide (the number in the parenthesis indicates the position of phosphorylation on the inositol moiety)
Conversely, patients who carry variants in hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13, rs72613567) and mitochondrial amidoxime-reducing component 1 (MARC1, rs2642438) are more protected than the general population (48, 49)
doi:10.2147/DMSO.S348025 113
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