Current lab members:
Lynne Cox (PI)
Adam Rolt (Elysium post-doctoral fellow)
Lukeriya Zharova (Part II MBiochem student)
Christopher Whiteman (DPhil student with Public Health England)
Thibault Teissier (BIRAX/Diabetes UK post-doctoral scientist)
Ivan Boubriak (UK SPINE postdoctoral scientist)
Recent lab members and new positions:
Hannah Walters (Humboldt post-doctoral Fellowship, Max Planck Insitute, Dresden, Germany)
Sebastian Aguiar (biotech, USA)
Hayley Lees (NHS Clinical Geneticist)
DPhil position available from next academic year:
We are looking to recruit a new DPhil student on a Cell Senscence and Ageing scholarship funded through the generosity of Jim Mellon and to be held at Oriel College, Oxford and the Department of Biochemistry. Please contact firstname.lastname@example.org with expressions of interest: a formal advertisement will be posted in due cousre (we are experiencing delays because of the COVID-19 emergency)
- Cox, LS. (2020) The Economic and Scientific Case for Therapeutic Intervention in Ageing. Key paper I (p72-80) in "Health of the Nation: a Strategy for Healthier Longer Lives", report of the APPG for Longevity, launched 12th February 2020, https://appg-longevity.org/events-publications
- Cox, L and Goljanek-Whysall, K (2019) Ageing here and now: current research and transformative therapies. Biogerontology 20: 249. https://doi.org/10.1007/s10522-019-09814-5
- Rolt, ACR, Nair, A and Cox, LS (2019) Optimisation of a screening platform for determining IL-6 associated inflammatory signalling in the senescence-associated secretory phenotype (SASP). Biogerontology https://doi.org/10.1007/s10522-019-09796-4
- Walters, HA and Cox, LS (2019) Generation of a novel model of primary human cell senescence through Tenovin-6 mediated inhibition of sirtuins. Biogerontology https://doi.org/10.1007/s10522-018-09792-0
- Walters, HW and Cox, LS (2018) mTORC Inhibitors as Broad-Spectrum Therapeutics for Age-Related Diseases Int J Mol Sci. 2018 Aug 8;19(8). pii: E2325. doi: 10.3390/ijms19082325.
- Chennuri, P, Cox, LS and Saunders, RDC. (2018) EXD2 and WRN exonucleases are required for interstrand crosslink repair in Drosophila. Preprint doi: https://doi.org/10.1101/284307
- Cox, LS, Mason PA. (2018) Towards understanding the biological drivers of cell ageing. Chapter 8 in The New Dynamics of ageing, volume 2. Ed Walker, A. Policy Press (Bristol) ISBN 978-1-4473-1479-0.
- Latorre E, Birar VC, Sheerin AN, Jeynes JCC, Hooper A, Dawe HR, Melzer D, Cox LS, Faragher RGA, Ostler EL, Harries LW. (2017) Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence. BMC Cell Biol. 2017 Oct 17;18(1):31. doi: 10.1186/s12860-017-0147-7.
- Cox, LS and Redman C. (2017) The role of cellular senescence in ageing of the placenta Placenta. 2017 Apr;52:139-145. doi: 10.1016/j.placenta.2017.01.116. Epub 2017.
- Lees H, Walters H, Cox LS. (2016) Animal and human models to understand ageing. Maturitas. 2016 Nov;93:18-27. doi: 10.1016/j.maturitas.2016.06.008.
- Alimbetov D, Davis T, Brook AJ, Cox LS, Faragher RG, Nurgozhin T, Zhumadilov Z, Kipling D. (2016) Suppression of the senescence-associated secretory phenotype (SASP) in human fibroblasts using small molecule inhibitors of p38 MAP kinase and MK2. Biogerontology. 2016 Apr;17(2):305-15. doi: 10.1007/s10522-015-9610-z.
- Walters HE, Deneka-Hannemann S, Cox LS. (2016) Reversal of phenotypes of cellular senescence by pan-mTOR inhibition. Aging (Albany NY). 2016 Feb;8(2):231-44.
#OSEF2020: Oxford Said Entrepreneurship Forum: Lynne was a speaker at in the Said Business Schools' annual flagship event, discussing "immortality"
Please note the planned Ageing Science seminar series for Trinity Term 2020 (https://www.archub.ox.ac.uk/2020/03/13/trinity-2020-seminar-series-pre-announcement/) has been postponed because of COVID-19. We hope to be able to run this exciting series of seminars by global leaders in the science of ageing in the future.
Healthy Ageing: From molecules to organisms: POSTPONED DUE TO COVID-19
27 - 29 May 2020 Wellcome Genome Campus, UK
The third conference in this series will focus on recent discoveries and current challenges in ageing research, with a focus on translating basic research insights into health improvement for older people.
Ageing can lead to declining health and function, and it is the major risk factor for cancer, neurodegenerative and cardiovascular disease. We aim to explore the mechanisms of ageing in cells, tissues and organisms in order to identify interventions that can ameliorate its negative effects.
The conference will focus on how recent developments in cell- and immune-senescence, neuroinflammation, stem cells and epigenetics are leading to an increased understanding of the ageing process. This year’s meeting will also highlight research into the ageing brain and nervous system and discuss lifestyle interventions for health improvement.
The meeting is aimed at scientists, clinicians and drug developers involved in research into ageing and other relevant fields.
What causes age-related disease and can ageing be treated?
Ageing and age-related diseases affect some people much more than others: there is no one fixed way to age and everyone is different. While we know that a good diet, exercise and plenty of sleep are important to maintain health, other factors out of our control (e.g. genes, environment) can lead to significant ill health and disability in later life. The vast majority of older people suffer from several chronic age-related diseases simultaneously - this is termed co-morbidity.
We now know that changes to cells as they age, termed cell senescence, can be critical in causing many different diseases of ageing. Exciting new research from labs around the world has shown that removing senescent cells can improve health in later life, and even extend lifespan in mice.
Cells undergo senescence in several different ways in response to DNA damage, activation of oncogenes or simply after they have undergone a large number of cell divisions until their telomeres (repetitive DNA structures at the ends of the chromosomes that shorten at every cell division cycle) have become critically short. Senescence is an important tumour suppressor mechanism to prevent damaged cells from dividing, but the many changes cells undergo as they become senescent leads to them altering their local environment, including degrading tissue structure and promoting a pro-inflammatory and pro-cancer environment.
By identifying the biochemical pathways and specific molecules involved, we aim to develop ways of altering the rate or outcomes of cell senescence, in order to better treat age-associated diseases and frailty.