Dr Rhian Thomas

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About me

Position: Senior Lecturer in Human Physiology

 

I am a Senior Lecturer in Human Physiology at UWE.  Prior to arriving at UWE in 2016 I worked as a Lecturer in Pharmacology and Physiology in the Cardiff School of Pharmacy and Pharmaceutical Sciences. I teach on the Biomedical Sciences and Healthcare Sciences programmes at UWE.  I am module leader for Anatomy and Physiology (FdSc, Healthcare Sciences, Level 1) and Practice and Communication of Sciences (Level 2) and co lead Neuropharmacology (Level 3).

Research Interests

My research has been directed at two main areas: cell signalling in disease and amyloid production in Alzheimer's disease (AD).  

There are two characteristic neuropathological features of AD, neurofibriallary tangles made of hyperphosphorylated tau and extracellular senile plaques made primarily of amyloid-beta, a 40-43 amino acid peptide produced from amyloid precursor protein (APP). An increase in amyloid-beta levels (especially amyloid-beta 42) is thought to be crucial for the pathogenesis of AD. Amyloid-beta is produced from the protein APP by cleavage events involving the enzymes beta- and gama-secretase which cleave APP sequentially to liberate amyloid-beta. Since the discovery of beta-secretase, an aspartic protease called beta-site APP-cleaving enzyme (BACE1) in 1999, there has been much interest in developing inhibitors.

My primary focus has been on investigating how amyloid-beta is produced in Alzheimer's disease, what affects this and developing therapies to influence this.  I am specifically interested in developing novel therapies and therapeutic antibodies for AD that inhibit amyloid-beta.

My current interests include the understanding of amyloid-beta generation, particularly in relation to the role of clathrin-dependent and -independent endocytosis and cell signalling pathways.

Area of expertise

Selected Other Publications:

Lowe, A.P.P., Thomas, R.S., Nials, A.T., Kidd, E.J., Broadley, K.J. and Ford, W.R. 2017. Route of Administration Affects Corticosteroid Sensitivity of a Combined Ovalbumin and Lipopolysaccharide Model of Asthma Exacerbation. Journal of Pharmacology and Experimental Therapeutics. DOI : 10.1124/jpet.117.241927

Lowe, A.P.P., Thomas, R.S., Nials, A.T., Ford, W.R., Kidd, E.J., and Broadley, K.J. 2015. Lipopolysaccharide exacerbates functional and inflammatory responses to ovalbumin and decreases sensitivity to inhaled fluticasone propionate in a model of asthma. British Journal of Pharmacology. 172(10), 2588-2603.

Thomas, R.S., Hvoslef-Eide, M., Good, M.A. and Kidd, E.J. 2013. Inhibition of amyloid-beta production by anti-amyloid precursor antibodies in mouse cortical neurones. NeuroReport. 24(18), 1058-61.

Blain, E.J., Thomas, R.S. and Duance, V.C. 2012. Effect of Wnt3A on load-induced markers of chondrocyte matrix metabolism. International Journal of Experimental Pathology 93 (4), A13-A14.

Thomas, R.S., Clarke, A.R., Duance, V.C and Blain, E. 2011. Effects of Wnt3A and mechanical load on cartilage chondrocyte homeostasis. Arthritis Research and Therapy 13:R203. doi:10.1186/ar3536. R203 file

Thomas, R.S., Lelos, M.J., Good M.A and Kidd, E.J. 2011. Clathrin-mediated endocytic proteins are upregulated in the cortex of the Tg2576 mouse model of Alzheimer's diseaselike amyloid pathology. Biochemical and Biophysical Research Communications. 415(4), 656-661.

Lelos, M.J., Thomas, R.S., Kidd, E.J. and Good M. 2011. Outcome-specific satiety reveals a deficit in context-outcome but not stimulus- or action-outcome associations in aged Tg2576 mice. Behavioral Neuroscience. 125, 412-425.

Thomas, R.S., Liddell, J.E. and Kidd, E.J. 2011. Anti-amyloid-beta-precursor protein antibodies inhibit amyloid-beta production by steric hindrance. FEBS Journal. 278, 167-178.

Thomas, R.S and Kidd, E.J. 2010. Targeting amyloid production with antibodies. Alzheimer's Society Research Newsletter. Quality Research in Dementia. February 2010:95 pp10

 

 

 

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