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Tau Protein and its Phosphorylation: Alzheimer?s Disease

Sunil Kumar Singh, Nisha Dhama, Arif Khan, Gaurav Singh

The alterations of insulin signaling, calcium signaling, mitochondrial deterioration and oxidative strain have been associated in the hyperphosphorylation of tau protein found in Downs syndrome dementia. Such sorts of pathogenic etiologies have clear ramifications in the counteractive action and treatment of Down's disorder (DS) dementia. The event of methylation abandons in DS is examined yet despite the fact that dubious, later studies do show criticalness. Kinases, for example, DYK1A and GlcNAcylation are examined and a Cdk5 inhibitory peptide (CIP). Indeed, even rest drug has been shown in that seniors, who have better rest, endure less subjective decay than those with slumber issues with upgraded leeway of β amyloid and tau neurofibrillary tangles. Studies have reported a high rate of slumber issues in Down's. Ecological poison arsenite and low dosage methyl mercury have been conjectured to prompt tau phosphorylation. Dietary changes to low glycemic carb and gluten shirking ought to be made. Including B vitamins may be similarly critical to avert cerebrum decay particularly in those with MTHFR and MTRR quality deformities. The remedial system of diminishing insulin resistance by up regulation of PPARS alpha with glitazones and diminishing calcium inundation into the mitochondria is said. Shielding mitochondrial decrease from oxidative anxiety with cancer prevention agents, and treatment with CBD, polyphenols, ellagic corrosive, resveratrol and other grape bioflavinoids and moderate attractive fields is examined.