Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Inherited mutations to the tumor suppressor PTEN sporadically lead to cerebellar gangliocytoma characterized by migration defects. This has been modeled by CNS-specific PTEN ablation in mice, but the underlying mechanism cannot be explained by the known role of PTEN in Akt/PKB inactivation. Here we show that the loss of PTEN in mouse cerebellar neurons causes neurodegeneration by hyperphosphorylation of tau and neurofilaments, and activation of Cdk5 and pERK1/2, suggesting that dysregulation of the PTEN/pAkt pathway can mediate neurodegeneration.

Original publication




Journal article


Mol Cell Neurosci

Publication Date





400 - 408


Analysis of Variance, Animals, Animals, Newborn, Blotting, Western, Cell Count, Cerebellum, Cyclin-Dependent Kinase 5, Enzyme Activation, Gene Expression Regulation, Developmental, Immunohistochemistry, Mice, Mice, Knockout, Mitogen-Activated Protein Kinase 3, Neurofilament Proteins, Neurons, PTEN Phosphohydrolase, Phosphorylation, tau Proteins