Targeting mTOR restores tau-induced metabolic, mitochondrial, and cognitive deficits in a tauopathy mouse model
What this study shows
In mice engineered to overexpress a phosphomimetic tau variant, one week of rapamycin partially mitigated tau-driven mitochondrial dysfunction and cognitive impairment in the Morris water maze - extends the mTOR-autophagy-neurodegeneration link (already seen with Huntington's) to a direct tau-phosphorylation mechanism relevant to Alzheimer's.
At a glance
| Evidence type | PP Preprint, not peer-reviewed This is a preprint, not yet peer-reviewed -- treat its findings as provisional until formal publication. Preprints carry their own marker because peer-review status is a different question from which system was studied. |
| Study type | Preprint |
| Model system | Mouse (Tau3E-overexpressing, hippocampal CA3) |
| Journal | bioRxiv (preprint) |
| Year | 2024 |
| Peer reviewed | No |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1101/2024.11.24.625068 |
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 (mTOR inhibition) |
| Target | mTOR / Tau (Ser214/Ser356/Thr231) |
| Model | Mouse (tauopathy, Tau3E CA3) |
| Effect | Targeting mTOR restores tau-induced metabolic, mitochondrial and cognitive deficits in a tauopathy 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.
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