Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice

Zhou J, Blundell J, Ogawa S, Kwon CH, Zhang W, Sinton C, Powell CM, Parada LF · 2009 · The Journal of neuroscience · Atlas ID ZHO2009

What this study shows

In neural Pten-knockout mice, rapamycin prevented and reversed neuronal hypertrophy and improved a subset of the PTEN-associated abnormal behaviours.

Abstract

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PTEN (phosphatase and tensin homolog deleted on chromosome ten) is a lipid phosphatase that counteracts the function of phosphatidylinositol-3 kinase (PI3K). Loss of function of PTEN results in constitutive activation of AKT and downstream effectors and correlates with many human cancers, as well as various brain disorders, including macrocephaly, seizures, Lhermitte-Duclos disease, and autism. We previously generated a conditional Pten knock-out mouse line with Pten loss in limited postmitotic neurons in the cortex and hippocampus.

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At a glance

Evidence type	A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse (Pten KO)); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Mouse (Pten KO)
Journal	The Journal of neuroscience
Year	2009
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1523/JNEUROSCI.5685-08.2009 · PMID 19211884 · Free full text (PMC3904448)

Extracted findings

These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.

Intervention	mTORC1 inhibition (rapamycin)
Target	mTORC1 / PTEN-Akt
Model	Mouse (neural Pten KO)
Effect	mTORC1 inhibition prevents and reverses neuronal hypertrophy in Pten-null brain and ameliorates a subset of PTEN-associated abnormal behaviours

In the Atlas

Open questions that cite this study

Cited as supporting evidence for the open question Brain-penetrant mTOR inhibition clears aggregates in models, but human dosing has not been shown to reach the brain — and mTORC2 is needed for memory in mice.

Cite this paper

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Zhou, J., Blundell, J., Ogawa, S., Kwon, C. H., Zhang, W., Sinton, C., Powell, C. M., & Parada, L. F. (2009). Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice. The Journal of neuroscience. https://doi.org/10.1523/JNEUROSCI.5685-08.2009

@article{ZHO2009,
  author       = {Zhou, J. and Blundell, J. and Ogawa, S. and Kwon, C. H. and Zhang, W. and Sinton, C. and Powell, C. M. and Parada, L. F.},
  title        = {{Pharmacological inhibition of mTORC1 suppresses anatomical, cellular, and behavioral abnormalities in neural-specific Pten knock-out mice}},
  journal      = {The Journal of neuroscience},
  year         = {2009},
  doi          = {10.1523/JNEUROSCI.5685-08.2009},
  note         = {PMID: 19211884},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record ZHO2009) [Data set]. https://mtor-atlas.org/study/ZHO2009/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_ZHO2009,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record ZHO2009},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/ZHO2009/},
  doi          = {10.5281/zenodo.22059963}
}

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