GSK-3α regulates production of Alzheimer's disease amyloid-β peptides

By C. Phiel, Christina A. Wilson, V. Lee, P. S. Klein. Nature, 2003

1,124 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/5b3bd73ef30c29ac9a47eb9a4d1cfb7d625a4586

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. D. Holtzman
2. D. Schoepp
3. M. Goedert
4. C. Zhong
5. Zhichun Chen

In Molecular Biology

1. Eléonore Beurel
2. M. Goedert
3. R. Jope
4. S. Grieco
5. A. D. Kohn
6. D. Schoepp
7. C. Zhong
8. D. Holtzman

In Physiology

1. D. Holtzman
2. M. Goedert
3. C. Zhong
4. Zhichun Chen
5. M. Finn
6. John R. Cirrito
7. D. Selkoe
8. J. Long

Citations in the corpus

• Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics (2007, background): “Abnormal accumulation of Aβ is a critical early stage in AD neuropathology, and several studies have shown that Aβ production is promoted by GSK3 and reduced by GSK3 inhibitors [67–70].”
• GSK3 inhibitors: development and therapeutic potential (2004, background): “Recent work has shown that GSK3 increases β-amyloid production, and that lithium chloride and kenpaullone can reduce Aβ level”
• WNT and β-catenin signalling: diseases and therapies (2004, background): “or compounds that mimic its activity, such as the GSK3 inhibitor, lithiu”
• Synaptic activity regulates interstitial fluid amyloid-beta levels in vivo. (2005, background): “Thus, it is likely that these drugs might influence Ab levels within specific neuronal networks as well (Phiel et al., 2003).”
• Alzheimer’s disease: pathogenesis, diagnostics, and therapeutics (2019, background): “Lithium and kenpaullone (two GSK3 inhibitors) prevent GSK3 expression and contribute to inhibition of Aβ production.(28) As such, GSK3 inhibitors might”
• Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “Furthermore, the studies have demonstrated that GSK-3a has been demonstrated to modulate APP cleavage and induce Ab production (Phiel et al., 2003; Sun et al., 2002), and that blockade of GSK-3b could prevent Ab accumulation (Alvarez et al., 1999; Takashima et al., 1993).”
• Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases (2014, background): “In Alzheimer’s disease, GSK3 has been demonstrated to promote every major pathological process, including amyloid β peptide production (Phiel et al., 2003) and tau phosphorylation (Himmelstein et al.”
• The GSK3 hypothesis of Alzheimer's disease (2008, background): “GSK3a, but not GSK3b, has been shown to regulate APP cleavage resulting in the increased production of Ab (Sun et al. 2002; Phiel et al. 2003).”