Hyperphosphorylation of microtubule-associated protein tau: a promising therapeutic target for Alzheimer disease.
By C. Gong, Khadija Iqbal. Current Medicinal Chemistry, 2008
613 citations recorded by the source corpus.
Subfields: Cell Biology, Cellular and Molecular Neuroscience, Physiology
View Paper: https://www.semanticscholar.org/paper/3166f167c07cd7a36ea02d4645743b31c895ad00
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In Cellular and Molecular Neuroscience
In Physiology
Citations in the corpus
- Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease (2011, background): “, decreasing kinase activities (for example, of glycogen synthase kinase-3”
- Post-translational modifications of tau protein: implications for Alzheimer's disease. (2011, neutral): “Overexpression of pseudophosphorylated tau has been reported to reduce microtubule interactions, to disrupt the microtubule network and to exert a neurotoxic effect (Cho and Johnson, 2004b; Fath et al., 2002; Gong and Iqbal, 2008; Zhang et al., 2009b).”
- Metals, oxidative stress and neurodegenerative disorders (2010, neutral): “Since the Ab42 levels are higher in AD patients, it was proposed that increased levels of Ab42 trigger the cascade of the deleterious events described above [6, 97, 98].”