1 , it is shown that GSK3 can be activated by the presence of beta amyloid, that can interfere with insulin [31] or Wnt [23] pathways; or could be activated by the presence of ps-1 mutations that alter the cadherin-PI-3 kinase pathway yielding an increase in GSK3 kinase activity [7] , [9] . Hemmings et al., 1981), Glycogen Synthase Kinase 3 (GSK-3) is by no means restricted to a role in glycogen metabolism. In Fig. Thus, other factors may explain how mutations in those genes result in the appearance of …
According to this hypothesis, over-activity of GSK3 accounts for memory impairment, tau hyper-phosphorylation, increased β-amyloid production and local plaque-associated microglial-mediated … Mutations in app, ps-1 and ps-2 genes result in the appearance of Familial Alzheimer disease (FAD). The GSK3 hypothesis of Alzheimers’ disease Recently, in an article published with this very same title [89] , it was proposed that the over activity of GSK3 accounts for memory impairment, tau phosphorylation, increased amyloid production and microglia-mediated inflammation, all features of AD. In summary , we suggest that GSK3 may play an important role in Alzheimer disease. GSK3 also plays a pivotal and central role in the pathogenesis of both sporadic and familial forms of Alzheimer's disease (AD), an observation that has led us to coin the ‘GSK3 hypothesis of AD’. Although, in many cases, those mutations result in an increase of the amount of beta amyloid peptide, there is not a clear correlation between that amount and the time of the onset of the disease. Glycogen synthase kinase-3β (microtubule associated kinase) plays a role in the phosphorylation of tau protein. Indeed, the enzyme targets a wide variety of proteins involved in signalling…
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