Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo.

By Wendy Noble, E. Planel, C. Zehr, Vicki Olm, J. Meyerson, Farhana Suleman, Kate Gaynor, Lili Wang, J. Lafrancois, Boris Feinstein and 7 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

733 citations recorded by the source corpus.

Subfields: Molecular Biology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/aa08261703d4368ca738982e9f849167657bd0cd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Eléonore Beurel
2. L. Ittner
3. John Q. Trojanowski
4. J. Götz
5. John Hardy
6. V. Lee
7. C. Zhong
8. Zhichun Chen

In Pharmacology

1. J. Götz
2. L. Ittner
3. E. Mandelkow

In Physiology

1. L. Ittner
2. J. Götz
3. V. Lee
4. John Q. Trojanowski
5. Wendy Noble
6. John Hardy
7. C. Zhong
8. Zhichun Chen

Citations in the corpus

• The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal (2009, background): “Additionally, it makes sense to pursue other targets beyond Ab (Noble et al. 2005).”
• Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics (2007, background): “GSK3 can also regulate the splicing of tau [96], hyperphosphorylated tau itself can be neurotoxic [97], and inhibition of GSK3 protects cells from aggregated tau-induced neurotoxicity [98].”
• 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”
• The GSK3 hypothesis of Alzheimer's disease (2008, background): “some of the pathological effects of over-expression of mutated APP and tau in the best available models of AD (Noble et al. 2005; Rockenstein et al. 2007).”
• Therapeutics of Alzheimer's disease: Past, present and future. (2014, background): “Lithium and valproate have inhibitory actions on GSK3 and when administered they reduce tau pathology in transgenic mice (Engel et al., 2006; Noble et al., 2005).”
• Post-translational modifications of tau protein: implications for Alzheimer's disease. (2011, unknown): “…transgenic mice, inhibition of GSK3b reduces tau phosphorylation (Caccamo et al., 2007; Engel et al., 2006; Nakashima et al., 2005), tauopathy and neurodegeneration (Noble et al., 2005), blocks NFT formation (Engel et al., 2006; Leroy et al., 2010) and rescues neuronal loss (Sereno et al., 2009).”
• Tau phosphorylation: the therapeutic challenge for neurodegenerative disease. (2009, background): “For example, inhibiting GSK-3 in tangle-forming transgenic mice reduces tau phosphorylation, insoluble tau load and neurodegeneration [ 19 ,20].”
• Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “, 1999) and tau hyperphosphorylation hypothesis (Noble et al., 2005).”
• Tau-mediated neurodegeneration in Alzheimer's disease and related disorders (2007, result): “For example, inhibition of GSK3 by lithium not only reduced tau phosphorylation in vivo , but also lowered the level of aggregated tau, compared with control”