Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis
What this study shows
Rapamycin reverses learning and memory deficits in a Tsc2+/- tuberous sclerosis model.
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 (Tsc2+/-)); 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 (Tsc2+/-) |
| Journal | Nature medicine |
| Year | 2008 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/nm1788 · PMID 18568033 · Free full text (PMC2664098) |
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 | Rapamycin (in Tsc2+/- mice) |
| Target | mTORC1 / TSC2 |
| Model | Mouse (Tsc2+/-) |
| Effect | mTOR inhibition reverses learning and memory deficits in a tuberous sclerosis mouse model |
In the Atlas
Related topics
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.
More studies on this topic
- Translational control of long-lasting synaptic plasticity and memory (2009)
- Chronic inhibition of mammalian target of rapamycin by rapamycin modulates cognitive and non-cognitive components of behavior throughout lifespan in mice. (2012)
- mTORC2 controls actin polymerization required for consolidation of long-term memory (2013)
- Aberrant excitatory neuronal ERBB4 promotes Alzheimer's disease pathology (2026)
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