Prof Jonathan Seckl
A clinical endocrinologist and former Wellcome Trust Senior Clinical Research Fellow, Prof Seckl’s research focuses on glucocorticoid biology from ‘cloning to clinic’.
- Vice Principal (Planning, Resources and Research Policy) 2012 - present
- Executive Dean (Medicine ) 2010 - present
- Director (Dean) of Research, College of Medicine and Veterinary Medicine (2005 - 2012)
- Moncrieff-Arnott Professor of Molecular Medicine, University of Edinburgh (1997 - present)
- Honorary Consultant Physician, NHS Lothian (1989 - present)
- Professor of Endocrinology, Edinburgh University, 1996 - 1997
- Wellcome Senior Clinical Fellow, Edinburgh University, 1989 - 1997
- PhD (Neuroendocrinology), London University, 1989
- MBBS, London University, 1980
- BSc (Zoology), London University, 1977
Prof Seckl led the new-build interdisciplinary Molecular Medicine Centre (130 researchers), set up the interdisciplinary Centre for the Study of the Ageing Brain (now an MRC Centre which he co-directs), was inaugural Head of School of Molecular and Clinical Medicine (500 staff), Director of Research for the College of Medicine and Veterinary Medicine (>2000 staff) and is currently Vice Principal at the University of Edinburgh.
Seckl coordinated the University’s submission to REF2014 and leads estates strategy and research planning.
Extramurally, Seckl has been on grant awarding committees for the Medical Research Council (MRC), Wellcome Trust, Royal Society of Edinburgh (RSE), other UK charities and the EU and was a member of the Scottish Government’s Scientific Advisory Committee and a 2008 Research Assessment Exercise (RAE2008) subpanel.
He currently co-chairs the Wellcome Trust core interview panel and the TSB-MRC Biomedical Catalyst Major Awards Committee. He has been elected to the Councils of the Academy of Medical Sciences and the Society for Endocrinology.
Seckl has authored over 340 peer-reviewed scientific papers (career citations >29,000, h=88). He has given over 200 invited lectures at international meetings including many plenary talks.
He has also talked to schools, lay audiences and in public fora (including BBC2’s Horizon) on stress, developmental programming and brain ageing.
41 of Seckl’s students have gained PhDs; many hold important positions in academia, industry and leadership across the globe.
Seckl holds patents in the fields of ageing and diabetes/obesity and has led drug discovery in an academic setting; one molecule has recently entered clinical trials.
He advanced the ‘Entrepreneur-in-Residence concept in a UK Medical School and leads Edinburgh’s MRC Developmental Pathway Funding Scheme Portfolio and its Confidence-in-Concept awards.
Jonathan Seckl is both medically and scientifically trained (MBBS at UCL, PhD in neuroendocrinology at Imperial College London).
A clinical endocrinologist and former Wellcome Trust Senior Clinical Research Fellow, Seckl’s research focuses on glucocorticoid biology from ‘cloning to clinic’.
He has been funded by four successive programme grants from the Wellcome Trust, and additional programme awards from Medical Research Council (MRC) and Human Frontier Science Program (HFSP).
The laboratory exploits technologies from molecular and cell biology through models in vivo to detailed clinical investigation.
The main themes are the discovery and understanding of the importance of local tissue inactivation/regeneration of glucocorticoids (by 11ß-hydroxysteroid dehydrogenases) as a cause of and therapeutic target for age-related memory impairments and the metabolic syndrome-diabetes-obesity continuum.
The group also advanced and supported the glucocorticoid hypothesis of fetal ‘programming’ and has elucidated fundamental molecular and epigenetic mechanisms by which this leads to subsequent disorders in adult life.
Our research is supported by external grant funding of ~£2 million per annum including current Programme Grants from Wellcome Trust, British Heart Foundation, and Medical Research Council.
And also a current HFSP programme award with colleagues in Canada and the Netherlands.
- Prof Brian Walker
- Prof Karen Chapman
- Dr Chris Kenyon
- Prof Megan Holmes
- Dr Roger Brown
- Dr Ruth Andrew
- Dr Moffat Nyirenda
- Dr Rebecca Reynolds
- Dr Paddy Hadoke
- Dr Nik Morton
- Dr Scott Webster
- Dr Mandy Drake
- Prof Alasdair MacLullich
- Dr Pauline Jamieson
- Dr Kerry McInnes
- Dr Joyce Yau
- Shareen Forbes
- Tiina Kapari
- Cristina Esteves
- Lizzy Cottrell
- Angie Harris
- Agnes Coutinho
- Caitlin Wyrwoll
- Professor Michael Meaney (McGill)
- Professor Jeff Flier (Harvard)
- Professor Bart Staels (Lille)
- Professor Bruce McEwen (Rockefeller)
- Professor Matt Gillman (Harvard)
- Professor Naomi Levitt (Cape Town)
- Professor Tommy Olsson (Umea)
- Professor Hannele Yki-Jarvinen (Helsinki)
- Professor Bernadette Breant (Paris)
- Professor Eberhard Fuchs (Gottingen)
- Professor Ron de Kloet (Leiden)
- Professor Rachel Yehuda (Mt Sinai, New York)
- Professor Alon Chen (Weizmann)
- Professor Julia Goedecke (Cape Town)
- Professor John Connell (Glasgow)
- Professor Inga Neumann (Regensburg)
Chapagain A, Caton PW, Kieswich J, Andrikopoulos P, Nayuni NK, Long J, Harwood S, Webster SP, Raftery MJ, Thiemermann C, Walker BR, Seckl JR, Corder R, Yaqoob MM (2014). Elevated hepatic 11β-hydroxysteroid dehydrogenase type-1 induces insulin resistance in uremia. PNAS USA 111:3817-22.
Kipari T, Hadoke PW, Iqbal J, Man TY, Miller E, Coutinho AE, Zhang Z, Sullivan KM, Mitic T, Livingstone DE, Schrecker C, Samuel K, White CI, Bouhlel MA, Chinetti-Gbaguidi G, Staels B, Andrew R, Walker BR, Savill JS, Chapman KE, Seckl JR (2013). 11β-hydroxysteroid dehydrogenase type 1 deficiency in bone marrow-derived cells reduces atherosclerosis. FASEB J 27:1519-31.
Cottrell EC, Holmes MC, Livingstone DE, Kenyon CJ, Seckl JR (2012). Reconciling the nutritional and glucocorticoid hypotheses of fetal programming. FASEB J 26:1866-74.
Turban S, Liu X, Ramage L, Webster SP, Walker BR, Dunbar DR, Mullins JJ, Seckl JR, Morton NM (2012). Optimal elevation of β-cell 11β-HSD1 is a compensatory mechanism that prevents high fat diet-induced β-cell failure. Diabetes 61:642-52
Michailidou Z, Turban S, Miller E, Xiantong Z, Schrade J, Ratcliffe PJ, Hadoke PW, Walker BR, Iredale JP, Morton NM, Seckl JR (2012). Increased angiogenesis protects against adipose hypoxia and fibrosis in metabolic disease-resistant 11β-hydroxysteroid dehydrogenase type 1 deficient mice. J Biol Chem 287:4188-97
Drake AJ, Liu L, Kerrigan D, Meehan RR, Seckl JR (2011). Multigenerational programming in the glucocorticoid programmed rat is associated with generation-specific and parent of origin effects. Epigenetics 6:1334-43
Yau JLW, Noble J, Seckl JR (2011). 11β-hydroxysteroid dehydrogenase type 1 deficiency prevents memory deficits with aging by switching from glucocorticoid receptor to mineralocorticoid receptor-mediated cognitive control. J Neurosci 31:4188-93.
MacLullich AMJ, Ferguson KJ, Reid LM, Deary IJ, Starr JM, Wardlaw JM, Walker BR, Andrew R, Seckl JR (2012). 11ß-Hydroxysteroid dehydrogenase type 1, brain atrophy and cognitive decline. Neurobiol Aging 33:207.e1-8.
Sooy K, Webster S, Noble J, Binnie M, Walker BR, Seckl JR and Yau JLW (2010). Partial deficiency or short-term inhibition of 11β-hydroxysteroid dehydrogenase type 1 improves cognitive function in ageing mice. J Neurosci 30: 13867-72.
Lucassen PJ, Bosch OJ, Jousma E, Krömer SA, Andrew R, Seckl JR, Neumann ID (2009). Prenatal stress reduces postnatal neurogenesis in rats selectively bred for high, but not low, anxiety: possible key role of placental 11β-hydroxysteroid dehydrogenase type 2. European Journal of Neuroscience 29: 97-103.
Wyrwoll CS, Seckl JR, Holmes MC (2009). Altered placental function of 11β-HSD2 knockout mice. Endocrinology 150:1287-93.
Yehuda R, Bierer LM, Andrew R, Schmeidler J, Seckl JR (2009). Enduring effects of severe developmental adversity, including nutritional deprivation, on cortisol metabolism in aging Holocaust survivors. Journal of Psychiatric Researcg 43:877-83.
de Vries A, Hazlewood L, Fitch PM, Seckl JR, Foster P, Howie SE (2009). High-fat feeding redirects cytokine responses and decreases allergic airway eosinophilia. Clinical & Experimental Allergy 39: 731-739.