Ben Pickard obtained a BSc in Biochemistry from Imperial College London (1992), and a PhD from the University of Edinburgh (1996). Before coming to the University of Strathclyde, he worked at the Babraham Institute, Cambridge on factors regulating DNA methylation, and at the Molecular Medicine Centre, Edinburgh, identifying genetic risk factors for common psychiatric illnesses such as schizophrenia, bipolar disorder and major depression.

• Teaching across Biomedical Sciences classes: BM110, 108, 109, 210, 214, 321, 326, 327, 422, 423, 430, 432; Pharmacy: MP422; Postgraduate: BM934, 937, 951, 942, 952, 953, 959.
• Coordinator of Biomedical Sciences classes BM321, BM423; Postgraduate: BM934, 937, 952.
• Personal Development Advisor
• Internal/external examiner PhD theses
• External examiner MSc Neuroscience, UCL, (2013-2015)

Certificates of Recognition in University of Strathclyde Student Union Teaching Excellence Awards: 2012, 2013, 2014. Winner: Most Supportive Teacher 2017.

The traditional view is that gene expression is largely governed by promoter activity, meaning that analysis is carried out gene-by-gene. Expressed mRNAs encode expressed proteins and, again, the prevailing view is that mRNA levels are the major influence on levels of their encoded proteins.

I have discovered an entirely new level of regulation for both mRNA and protein expression that is based on the idea that the synthesis of both types of molecules is dependent on an interaction between the supply of building blocks (nucleotides or amino acids) and the demands of the sequences of the mRNAs or proteins to be made (how extreme/costly a composition they possess). Independent studies of protein expression data, and now mRNA expression data, have shown that this interaction drives a global-level regulation of expression. This is like looking at the 'wood' instead of the 'trees', and offers a high-level readout of the cellular state.

For proteins, we have shown that growth/cell proliferation eats up the amino acid supply, particularly limiting the expression of  proteins involved in connective tissue structure. For mRNA, the situation much more profound. I see global mRNA expression profiles shifted in numerous disease states such as Alzheimer's disease , schizophrenia, and autoimmune conditions. Additionally, 20% of all drugs/chemicals assessed perturb the global profile, revealing a new way to think of drug action and side-effect. It's not all pathological: the cell uses this form of regulation across the circadian day and menstrual cycle, and it apears to correlate with the extent of cellular differentiation. In fact, cells appear to use changes in nucleobase supply to shift their global expression profile as an efficent way to reprogram physiological state or to respond to adversity.

The goal of my research now is to convert these largely data-driven findings into practical applications relating to disease understanding and treatment.