Oliver's mTOR Atlas Evidence Platform
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Rapamycin improves healthspan but not inflammaging in nfκb1(-/-) mice.

Correia-Melo C, Birch J, Fielder E, Rahmatika D, Taylor J, Chapman J, Lagnado A, Carroll BM, Miwa S, Richardson G, Jurk D, …, Passos JF · 2018 · Aging Cell · Atlas ID COR2018

What this study shows

Separates two effects of rapamycin that are usually assumed to travel together. In mice with genetically enhanced NF-kB activity, rapamycin showed no benefit in lifespan and no reduction of inflammaging, yet still reduced frailty and improved long-term memory, neuromuscular coordination and tissue architecture, with lower markers of cellular senescence. Healthspan benefit is therefore uncoupled here from suppression of inflammation, which is a boundary condition on the common claim that rapamycin acts on ageing mainly by damping inflammation. Note the mixed result: the healthspan outcomes are positive, the lifespan and inflammaging outcomes are null.

Abstract

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Increased activation of the major pro-inflammatory NF-κB pathway leads to numerous age-related diseases, including chronic liver disease (CLD). Rapamycin, an inhibitor of mTOR, extends lifespan and healthspan, potentially via suppression of inflammaging, a process which is partially dependent on NF-κB signalling. However, it is unknown if rapamycin has beneficial effects in the context of compromised NF-κB signalling, such as that which occurs in several age-related chronic diseases.

Read the full abstract on PubMed →

At a glance

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Evidence type A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: nfkb1-knockout mice (genetically enhanced NF-kB activity, low-grade chronic inflammation, accelerated ageing); dietary rapamycin); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type4 - Animal Study
Model systemnfkb1-knockout mice (genetically enhanced NF-kB activity, low-grade chronic inflammation, accelerated ageing); dietary rapamycin
JournalAging Cell
Year2018
Peer reviewedYes
Record last updated2026-10-01
SourceDOI 10.1111/acel.12882 · PMID 30468013

Where this study fits

How this study connects to the pathway map, open questions, people and other studies in the Atlas.

Open question

Mechanism-to-outcome gap · H10

How much of rapamycin's healthspan benefit runs through fewer senescent cells?

Cited there as evidence. Evidence stands at: Mechanism in cells.

People in the Atlas

  • Clara Correia-Melo first author · 1 study in the Atlas

    Ageing biologist who showed with João Passos in Newcastle that rapamycin can improve healthspan in mice without lowering inflammation, and later studied metabolite sharing between cells in Markus Ralser's lab

  • João F. Passos last author · 1 study in the Atlas

    Studies how senescent cells, mitochondria and telomeres contribute to ageing and age-related disease.

  • Satomi Miwa 2 studies in the Atlas

    Mitochondrial biologist who contributed to Newcastle studies on rapamycin in NF-κB-driven ageing mice and on basal mitophagy as a brake on cellular senescence.

  • Viktor I. Korolchuk 5 studies in the Atlas

    Showed that where lysosomes sit inside the cell tunes mTORC1 activity to nutrient supply. His Newcastle lab found that senescent cells can no longer switch mTORC1 off when nutrients or growth factors are withdrawn, and studies how autophagy and mitophagy decline with age

More: 12 other authors

No profile yet: Birch J, Fielder E, Rahmatika D, Taylor J, Chapman J, Lagnado A, Carroll BM, Richardson G, Jurk D, Oakley F, Mann J, Mann DA

Related studies

More related studies

All 19 studies on Cellular senescence

Topics

Age-related pathologyCellular senescenceNF-κB

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.

InterventionDietary rapamycin
TargetmTOR (mTORC1)
ModelMouse (nfkb1-/-, enhanced NF-kB activity)
EffectRapamycin reduced frailty and senescence markers and improved memory and coordination, but did not extend lifespan or reduce inflammaging.

Cite this paper

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Correia-Melo, C., Birch, J., Fielder, E., Rahmatika, D., Taylor, J., Chapman, J., Lagnado, A., Carroll, B. M., Miwa, S., Richardson, G., Jurk, D., Oakley, F., Mann, J., Mann, D. A., Korolchuk, V. I., & Passos, J. F. (2018). Rapamycin improves healthspan but not inflammaging in nfκb1(-/-) mice. Aging Cell. https://doi.org/10.1111/acel.12882

@article{COR2018,
  author       = {Correia-Melo, C. and Birch, J. and Fielder, E. and Rahmatika, D. and Taylor, J. and Chapman, J. and Lagnado, A. and Carroll, B. M. and Miwa, S. and Richardson, G. and Jurk, D. and Oakley, F. and Mann, J. and Mann, D. A. and Korolchuk, V. I. and Passos, J. F.},
  title        = {{Rapamycin improves healthspan but not inflammaging in nfκb1(-/-) mice}},
  journal      = {Aging Cell},
  year         = {2018},
  doi          = {10.1111/acel.12882},
  note         = {PMID: 30468013},
}

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 COR2018) [Data set]. https://mtor-atlas.org/study/COR2018/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_COR2018,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record COR2018},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/COR2018/},
  doi          = {10.5281/zenodo.22059963}
}
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