Oliver's mTOR Atlas Evidence Platform
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Fiona Menzies

Cell biologist who worked for many years in David Rubinsztein's Cambridge lab on autophagy and the clearance of disease proteins in neurodegeneration

Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine (papers with David Rubinsztein, 2006–2021)

Fiona Menzies Portrait: LinkedIn

Fiona Menzies is a co-author on two Atlas papers from David Rubinsztein's lab. BER2006 showed in cultured cells that rapamycin, by switching on autophagy, the cell's self-cleaning system, helps clear several clumping proteins linked to brain disease and reduces their toxicity, and that it lowers toxicity of human tau in fruit flies. KOR2011 found that where the lysosome sits in the cell helps decide whether mTORC1, the growth-control complex, is on: with nutrients present lysosomes move to the cell edge and mTORC1 is active, while starvation pulls them towards the nucleus, mTORC1 falls and autophagy starts.

PubMed lists more than 40 papers that Menzies co-authored with Rubinsztein, from the mid-2000s to 2021, many on autophagy in neurodegenerative disease and on ways to raise autophagy with drugs or genetic tools. No current institutional page was found, so the affiliation shown is the one on the Atlas papers.

Milestones in the Atlas

A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.

YearEvidenceStudy
2006 M Rapamycin alleviates toxicity of different aggregate-prone proteins BER2006 Co-author on the paper showing that rapamycin reduces the toxicity of several aggregate-prone proteins in cells and of tau in flies.
2011 M Lysosomal positioning coordinates cellular nutrient responses KOR2011 Co-author on the paper showing that lysosome position inside the cell tunes mTORC1 activity and autophagy.

Co-authors in the Atlas 6

People with a profile here who share at least one study with Fiona Menzies.

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  • Cahir O'Kane 2 shared studies Fruit-fly geneticist at Cambridge who studies how the endoplasmic reticulum is built inside nerve fibres and how its failure causes hereditary spastic paraplegia, and who helped bring Drosophila models into David Rubinsztein's autophagy work
  • David C. Rubinsztein 2 shared studies Showed that rapamycin induces autophagy to clear the toxic protein of Huntington's disease, and that where lysosomes sit inside a cell helps set mTORC1 activity
  • Brinda Ravikumar First author of the 2004 study showing that switching off mTOR clears the toxic protein of Huntington disease by autophagy
  • Viktor I. Korolchuk 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
  • Vojo Deretic Studies how autophagy shapes infection, immunity and inflammation, including early work showing that autophagy restricts Mycobacterium tuberculosis, and how galectins and TRIM proteins control mTOR and AMPK.
  • Zdenek Berger Neuroscientist who, in David Rubinsztein's lab in Cambridge, showed that rapamycin-induced autophagy lowers the toxicity of several disease proteins that form clumps, including tau in fruit flies

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