Professor Stephen B Wharton
School of Medicine and Population Health
Professor and Honorary Consultant in Neuropathology


Full contact details
School of Medicine and Population Health
葫芦影业 Institute for Translational Neuroscience (SITraN)
385a Glossop Road
葫芦影业
S10 2HQ
- Profile
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- 2014 - present: Professor in Neuropathology, 葫芦影业
- 2001-2014: Senior Lecturer / Reader in Neuropathology, 葫芦影业
- 2001 鈥 present: honorary consultant in neuropathology, 葫芦影业 Teaching Hospitals
- 1997 - 2001: Senior lecturer / honorary consultant in Neuropathology, Edinburgh University
- 1994 鈥 1997: Senior registrar in Neuropathology, Addenbrookes Hospital, Cambridge
- Qualifications
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- PhD, University of 葫芦影业, 2013
- FRCPath awarded 2005
- MRCPath in Neuropathology 1997
- DipRCPath Histopathology 1995
- MSc University of Cambridge 1995
- MBBS London University 1988
- BSc (Hons) University of London 1985
- Research interests
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Professor Wharton鈥檚 research interest are focused on the cellular and molecular pathology of dementia and brain ageing. His major areas of interest are in:
- Lead in neuropathology for the which takes a population-based approach to understanding the pathological basis of late-life dementia.
- Investigating the cellular and molecular pathology of astrocytes, neurones and endothelium as components of the neurovascular unit in brain ageing and in the pathogenesis of dementia.
- The pathogenesis of white matter pathology in brain ageing and its contribution to dementia.
- The pathology of motor neurone diseases and tissue banking.
External collaborations
- Prof Fiona Matthews (University of Newcastle) and Prof Carol Brayne (University of Cambridge). The Cognitive Function and Ageing Study.
- Publications
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Journal articles
Chapters
Conference proceedings papers
Datasets
Preprints
- Research group
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Current PhD students:
- Harriet Brooke
Research team:
- Dr Bridget Ashford
- Dr Bridget Benson
- Mr Saif Ahamed
- Grants
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Current funding sources
- Alzheimer鈥檚 Society
- Alzheimer鈥檚 Research UK
- British Heart Foundation
- Teaching interests
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- Module leader: Neurodegeneration module, MSc Translational Neuroscience
- MSc lectures 鈥 Translational Neuroscience
- MBBS lectures 鈥 Preclinical neurosciences
- Neuroanatomy dissection teaching
- Supervisor SSC research projects
- Supervisor MSc research projects
- Seminars to postgraduate trainees in histopathology and clinical neurosciences
- Professional activities and memberships
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Editorial activities
- Consulting editor, Neuropathology and Applied Neurobiology (2014-7)
- Editor-in-Chief, Neuropathology and Applied Neurobiology (2007-13)
External professional activities 鈥 current and recent
- President of the British Neuropathological Society (2022 鈥 2024)
- Vice-president of the British Neuropathological Society (2020-2022)
- Member of the annual review panel for Brains for Dementia Research (2022 鈥 present)
- Member of the Alzheimer鈥檚 Research UK Grant Review Board 2016- 2022
- Chair of the specialist advisory committee in neuropathology, Royal College of Pathologists, 2020-2022
- Chief of panel of examiners in neuropathology for the Royal College of Pathologists (2018-21)
- Examiner in neuropathology for the Royal College of Pathologists (2005-21)
Membership of associations and societies - current
- International Society for Neuropathology
- British Neuropathological Society
- Current projects
Neuronal Senescence as a Contributory Mechanism to Dementia
Funded by Alzheimer's Research UK, this project aims to study the contribution of neuronal senescence to dementia. Markers of dementia, such as tangles and plaques that characterise Alzheimer鈥檚, do not explain all dementia, and treatments aimed at them have been unsuccessful. This suggests other processes contribute to dementia.
Senescent cells, sometimes called zombie cells, are persistently damaged cells, often because of damage to their DNA, which carries all the instructions for the cell. These cells remain alive, but they do not carry out their normal functions. Additionally, they produce factors that damage nearby cells and cause inflammation. Zombie cells are described in other tissues and diseases and there are drug treatments aimed at them. However, their role in dementia is not understood. Using brain tissue samples from the Cognitive Function and Ageing Study, we plan to identify senescent nerve cells in the brain and determine how they relate to dementia.
To determine how senescence causes damage, we will isolate nerve cells with and without markers of senescence from the same cases, and investigate effects on the cells by determining differences in the gene messages present. This will provide greater understanding of how senescence contributes to dementia and identify specific ways in which senescence affects nerve cells, which may lead us to new approaches to target zombie cells.
How does brain microvascular disease, especially pathological changes to capillaries, contribute to dementia?
Studies of blood vessel diseases, the second commonest cause of dementia, have focused mainly on large or small arteries. However, the contribution of pathology affecting the smallest vessels, the capillaries, is not understood. Brain capillaries are specialised to ensure that substances entering the brain from the blood are tightly-regulated and that blood supply is matched to the needs of nerve cells. This study, funded by the British Heart Foundation, will investigate the contribution of microvascular disease (MVD), affecting the capillaries, to dementia. Using donated human brain tissue, we will first characterise MVD using immunohistochemistry, a method that allows us to identify whether and where particular molecules are expressed and to measure them using a computer. Secondly, we will determine how these new MVD measures compare to other, existing measures of dementia-related pathologies. Thirdly, we will extend the assessment of the most informative MVD measures to all 550 donations, then determine how MVD contributes to dementia using advanced statistical methods. Lastly, we will identify potential new mechanisms of capillary damage by examining the expression of all the messages (mRNA) that code for protein production in the capillaries. Computer-based approaches will allow us to analyse this data to identify changes in cell processes that contribute to disease.
What is the Contribution of Basal Ganglia Pathology to Late-life Dementia and Frailty?
Most studies of dementia focused on the cerebral cortex, but other brain regions are also important. This PhD studentship, funded by the Alzheimer鈥檚 Society, aims to investigate how pathology in the basal ganglia contributes to dementia and frailty in late-life. The basal ganglia have many connections to the cortex and are involved in cognition as well as in motor control. They are affected by vascular disease and in the progression of Alzheimer鈥檚 disease. We plan to use human autopsy brain tissue samples donated as part of the Cognitive Function and Ageing Study. We will characterised vascular pathology and neurodegenerative pathology in basal ganglia using microscopy and immunohistochemistry. We will then determine the contribution that pathology in the basal ganglia makes to dementia and also to frailty. Finally, we will use gene expression analysis to determine new pathways by which pathology in basal ganglia might damage the function of this tissue.