| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Proctor, Carole J Gray, Douglas A |
| Abstract | Background Recent evidence suggests that glycogen synthase kinase-3β (GSK3β) is implicated in both sporadic and familial forms of Alzheimer's disease. The transcription factor, p53 also plays a role and has been linked to an increase in tau hyperphosphorylation although the effect is indirect. There is also evidence that GSK3β and p53 interact and that the activity of both proteins is increased as a result of this interaction. Under normal cellular conditions, p53 is kept at low levels by Mdm2 but when cells are stressed, p53 is stabilised and may then interact with GSK3β. We propose that this interaction has an important contribution to cellular outcomes and to test this hypothesis we developed a stochastic simulation model. Results The model predicts that high levels of DNA damage leads to increased activity of p53 and GSK3β and low levels of aggregation but if DNA damage is repaired, the aggregates are eventually cleared. The model also shows that over long periods of time, aggregates may start to form due to stochastic events leading to increased levels of ROS and damaged DNA. This is followed by increased activity of p53 and GSK3β and a vicious cycle ensues. Conclusions Since p53 and GSK3β are both involved in the apoptotic pathway, and GSK3β overactivity leads to increased levels of plaques and tangles, our model might explain the link between protein aggregation and neuronal loss in neurodegeneration. |
| Related Links | https://molecularneurodegeneration.biomedcentral.com/counter/pdf/10.1186/1750-1326-5-7.pdf |
| Ending Page | 15 |
| Page Count | 15 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 17501326 |
| DOI | 10.1186/1750-1326-5-7 |
| Journal | Molecular Neurodegeneration |
| Issue Number | 1 |
| Volume Number | 5 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2010-01-26 |
| Access Restriction | Open |
| Subject Keyword | Neurosciences Neurology Molecular Medicine System Biology Markup Language System Biology Markup Language Model Mdm2 Level Mdm2 mRNA Camptothecin Treatment |
| Content Type | Text |
| Resource Type | Article |
| Subject | Neurology (clinical) Molecular Biology Cellular and Molecular Neuroscience |
| Journal Impact Factor | 15.1/2023 |
| 5-Year Journal Impact Factor | 16.8/2023 |
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