Allzheimer disease

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by RohitM
Last updated 6 years ago

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Allzheimer disease

To test their hypothesis that sodium selenate does reduce tau phosphorylation, two independent tau transgenic mutant mice were given chronic oral treatment of sodium selenate. The two mutant strains were P301L mutant pR5 and K369I mutant K3 mice both of which exhibited reduced tau phosphorylation and completely rescinded NFT formation after chronic oral treatment. Furthermore, the effect of sodium selenate was also tested on the process of tau phosphorylation regulated by kinases and phosphotases.

One of the major phosphotases involved in tau dephosphorylation is protein phosphotase 2A (PP2A). PP2A is a serine/threonine specific protein phosphotase that has reduced activity and levels in an AD brain. The chronic oral treatment of sodium selenate also stabilized PP2A-tau complexes. However, PP2A seems to have a reduced role in tau pathology as dominant-negative mutant form of PP2A mice displayed an absence of any improvement when treated with sodium selenate. Therefore, sodium selenate appears to be a leading compound for tau-targeted treatments of AD as it has shown to reduce tau-pathology in several AD models.

Sodium Selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease models

Alzheimer's disease (AD) is a neurodegenerative disease most commonly characterized by continuous loss in regions of the cortex. The histopathology of AD involves β-Amyloid plaques in conjunction with intracellular neurofibrillary tangles (NFTs) which are a result of hyperphosphorylated tau protein. The authors in this study, have identified the compound sodium selenate to reduce tau phosphorylation in vitro and in vivo.

Sources - Alzheimer`s Disease vs Normal Brain - Protein Phosphatase Flow Chart - Neurofibrillary tangles - PET Scan - Brain Jigsaw PuzzleSodium Selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease - Two Graphs on Sodium Selenate


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