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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