The GSK3 hypothesis of Alzheimer's disease

By C. Hooper, R. Killick, S. Lovestone. Journal of Neurochemistry, 2008

1,166 citations recorded by the source corpus.

J. Neurochem. (2008) 104, 1433–1439.

Subfields: Genetics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/6112dd78b7f5bdfb9baa9f0cba7d90de6882da5f

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. John Q. Trojanowski
2. C. Zhong
3. Zhichun Chen

In Physiology

1. Julie A. Schneider
2. David A. Bennett
3. R. Wilson
4. Zoe Arvanitakis
5. John Q. Trojanowski
6. C. Zhong
7. Zhichun Chen
8. C. Iadecola

Citations in the corpus

• Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. (2012, background): “(55), asserts that GSK-3 is overactive in this disorder and accounts for its hallmark pathology, including τ hyperphosphorylation leading to NFT formation.”
• Recent advances in Alzheimer’s disease: mechanisms, clinical trials and new drug development strategies (2024, background): “333,338,339 mTORC1, a downstream molecule of Akt, also serves as a critical nexus linking insulin signaling with the autophagy system.”
• Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “Cumulative evidence has proved that GSK-3 increases tau phosphorylation, Ab aggregation, memory impairment, as well as microglia activation-associated inflammatory reactions in AD (Hooper et al., 2008).”