B.Sc Pharmacology (Hons) Graduate in 1985 (University of Bradford), PhD in Neuro Pharmacology 1990 (University of London). Joined Department of Pharmacology, Charing Cross & Westminster Medical School (Now part of Imperial College) as a lecturer in 1994. Current position - Professor in Neuropharmacology, Deputy Head Division of Brain Sciences and Scientific Director of Parkinson's UK Tissue Bank.
Research interests: Mechanisms of cell death and neuroprotection in Parkinson's Disease.
Parkinson’s disease (PD) is a common neurodegenerative movement disorder affecting 1 in 1000 of the general population and 1 in 100 of those aged over 60 years. The principle neuronal system that degenerates in PD is the nigrostriatal tract that uses dopamine as its neurotransmitter. Drug treatment mainly focuses on replacing the lost dopamine. Although there are several drugs on the market to treat PD these drugs are associated with long-term side effects and only treat the clinical symptoms of the disease and do not stop the remaining cells from dying.
In order to develop better treatment for PD we firstly must understand how the cells are dying in the disease. For over 27 years we have been investigating what possible mechanisms could contribute to the degeneration. We have been instrumental in providing evidence that the mechanisms of neurodegeneration includes oxidative stress, altered iron metabolism, mitochondrial dysfunction and neuroinflammation. The research group has a principle focus of undestanding the disease mechanisms and developing novel neuroprotective strategies.
Current research topics include:
- The development of antioxidants and metal chelators as neuroprotectory agents for treating Parkinson’s.
- Role of glutamate metabotropic receptor drugs in symptom amelioration and neuroprotection in Parkinson’s.
- Role of inflammation in the disease process and the beneficial effects of anti-inflammatory agents.
- Sex differences in the incidence of Parkinson’s disease and the neuroprotectory effects of estrogen.
- The involvement of stress in the development of Parkinson’s.
- Role of genetics, risk genes and Gene expression studies in Parkinson’s.
- Role of histone deacetylases (HDAC) in the neurodegenerative process in Parkinson’s and the potential use of HDAC-inhibitors.
- Development of nano-particles as drug delivery vehicles across the blood brain barrier
- Involvement of Calcium homeostasis in the neurodegenerative process in Parkinson’s
- Developing animal and cellular model of Parkinson’s.
The UK Parkinson’s Disease Society Tissue Bank
The Tissue Bank was established at Imperial College in January 2002, funded by a grant from the Parkinson’s Disease Society, to provide high quality post-mortem brain tissue to researchers in the UK. Tissue donation is via a prospective donor scheme that covers the whole of the UK. The Tissue Bank has also been instrumental in up dating the neuropathological diagnosis of PD by the inclusion of modern immunocytochemical techniques e.g. staining for alpha-synuclein, to help confirm the presence of PD as opposed to other PD like syndromes and dementia.
Funding research: Imperial College is a registered charity and we can accept direct funding to full or part fund a variety of project. For further details contact Dr Dexter
Harrison IF, Powell NM, Dexter DT, 2019, The histone deacetylase inhibitor nicotinamide exacerbates neurodegeneration in the lactacystin rat model of Parkinson's disease, Journal of Neurochemistry, Vol:148, ISSN:0022-3042, Pages:136-156
et al., 2019, L-DOPA functionalized, multi-branched gold nanoparticles as brain-targeted nano-vehicles, Nanomedicine: Nanotechnology, Biology and Medicine, Vol:15, ISSN:1549-9634, Pages:1-11
et al., The S100A4 protein signals through the ErbB4 receptor to promote neuronal survival., Theranostics, ISSN:1838-7640
et al., 2018, Iron as a therapeutic target for Parkinson's disease, Movement Disorders, Vol:33, ISSN:0885-3185, Pages:568-574
Harrison IF, Smith AD, Dexter DT, 2018, Pathological histone acetylation in Parkinson's disease: Neuroprotection and inhibition of microglial activation through SIRT 2 inhibition, Neuroscience Letters, Vol:666, ISSN:0304-3940, Pages:48-57