Author(s): Trent W Nichols
The changes of insulin signaling, calcium signaling, mitochondrial decline and oxidative stress have been implicated in the hyperphosphorylation of tau protein found in Downs syndrome dementia. Such pathogenic etiologies have clear implications in the prevention and therapy of Down’s syndrome (DS) dementia. The occurrence of methylation defects in DS is discussed and though controversial, more recent studies do show significance. Kinases such as DYK1A and GlcNA cylation are discussed as well as a Cdk5 inhibitory peptide (CIP). Even sleep medicine has been demonstrated in that seniors, who have better sleep, suffer less cognitive decline than those with sleep problems with enhanced clearance of β amyloid and tau neurofibrillary tangles. Studies have reported a high incidence of sleep problems in Down’s. Environmental toxin arsenite and low dose methyl mercury have been speculated to induce tau phosphorylation. Dietary changes to low glycemic carbohydrate and gluten avoidance should be made. Adding B vitamins may be equally important to prevent brain atrophy especially in those with MTHFR and MTRR gene defects. The therapeutic strategy of reducing insulin resistance by up regulation of PPARS alpha with glitazones and decreasing calcium influx into the mitochondria is mentioned. Protecting mitochondrial decline from oxidative stress with antioxidants, and treatment with CBD, polyphenols, ellagic acid, resveratrol and other grape bioflavinoids and moderate magnetic fields is discussed
