Dr Richard Tuxworth MA PhD

Dr Richard Tuxworth

Institute of Cancer and Genomic Sciences
Associate Professor
Head of Education

Contact details

Centre for Rare Diseases and Personalised Medicine
Institute of Cancer and Genomic Sciences
College of Medical and Dental Sciences
IBR West Extension Level 2
University of Birmingham
B15 2TT

Richard is an Associate Professor and Head of Education based in the Institute of Cancer and Genomic Sciences. He is a cell biologist with a particular interest in understanding DNA damage in neurological disease.


  • Associate fellow of the Higher Education Academy 2012
  • PhD (University of London), 1999
  • MA (Cantab), 1998
  • BA (Cantab) in Natural Sciences, 1994


Richard studied for a PhD in cell biology at the MRC Centre for Molecular Cell Biology at University College London with Robert Insall before moving to the University of Minnesota where he was a post-doctoral fellow with Meg Titus. He returned to the UK to work with Bill Chia and Guy Tear at the MRC Centre for Developmental Neurobiology at King's College London. In October 2012 Richard moved to the University of Birmingham as a Lecturer in Molecular Genetics in the School of Clinical and Experimental Medicine. He is now an Associate Professor and Head of Education in the Institute of Cancer and Genomic Sciences.


Postgraduate supervision

Richard currently supervises two PhD students. He is interested in supervising post-graduate students in the following areas: 

  • The molecular and cellular basis of neurodegeneration
  • The response of the nervous system to DNA damage
  • Drosophila models of disease
  • Lysosomal storage disorders and other inherited metabolic disorders
  • The function of lysosomes in neuronal health and disease
  • Stress signalling in neurons

If you are interested in studying any of these subject areas please contact Richard directly, or for any general doctoral research enquiries, please email mds-gradschool@contacts.bham.ac.uk


Richard Tuxworth is a cell biologist interested in disorders of the nervous system. He studies both early-onset inherited forms of neurodegeneration and the more common neurodegenerative disorders associated with old age. His laboratory is particularly interested in understanding how DNA damage impacts on nervous system function in neurological disease and finding out whether manipulating the response of cells to DNA damage could be used therapeutically.

DNA damage in neurological disease

Richard and colleagues in the College of Medical and Dental Sciences are investigating how accumulating DNA damage impacts on central nervous system function in chronic neurological diseases, such as Alzheimer’s diseases, and in acute neurological diseases, such after trauma. Richard’s group uses a combination of cell culture, biochemistry, genetics and genomics to understand the cell biology of neural responses to DNA damage and uses simple models of neurodegenerative disease developed in fruit flies to perform rapid surveys of potential new methods of intervention in neurological disease.

Lysosomal storage disorders and neural development

Lysosomes are low-pH organelles critical for recycling in cells and for coordination of growth and stress signalling. Lysosomes become dysfunctional in a large group of inherited syndromes known as the lysosomal storage disorders. Many result in neuropathology at a young age, including fatal childhood-onset neurodegeneration. The early pathology suggests lysosomal function must be essential for normal neuronal development. To study this, Richard’s group primarily use fruit flies as a simple model system to understand how and why the nervous system is sensitive to changes in lysosomal biology.

Birmingham Fly Facilityhttps://www.birmingham.ac.uk/research/birmingham-fly-facility/birmingham-fly-facility.aspx


Tuxworth, R., Taylor, M., Anduaga, A. M., Hussien-Ali, A., Chatzimatthaiou, S., Longland, J., Thompson, A. M., Almutiri, S., Alifragis, P., Kyriacou, C. P., Kysela, B. & Ahmed, Z. (2019) Attenuating the DNA damage response to double-strand breaks restores function in models of CNS neurodgeneration.  Brain Communications. 1, 1, 21 p., fcz005.

Taylor MJ, Thompson AM, Alhajlah S, Tuxworth RI, Ahmed Z. (2022) Inhibition of Chk2 promotes neuroprotection, axon regeneration, and functional recovery after CNS injury. Science Advances, vol. 8, eabq2611. https//doi: 10.1126/sciadv.abq2611.

Ahmed Z and Tuxworth RI (2022). The brain-penetrant ATM inhibitor, AZD1390, promotes axon regeneration and functional recovery in preclinical models of spinal cord injury. Clin Transl Med 2022. Jul; 12(7):e962 https://doi.org/10.1002/ctm2.962

Ahmed Z and Tuxworth RI (2022). Inhibiting the DNA damage response pathway promotes functional recovery after spinal cord injury. Clinical and Translational Discovery. Sept 2022. e106. https://doi.org/10.1002/ctd2.106

Faller K.M., Gutierrez-Quintana R., Mohammed A., Rahim, A.A., Tuxworth R.I., Wager K. and Bond M. (2015). The Neuronal Ceroid Lipofuscinoses: opportunities from model systems. Biophysica Biochemica Acta Molecular Basis of Disease. pii: S0925-4439(15)00128-3. doi:10.1016/j.bbadis.2015.04.022. PMID: 25937302

Povellato G., Tuxworth R.I., Hanger D.P. and Tear G. (2013). Modification of the Drosophila model of in vivo Tau toxicity reveals protective phosphorylation by GSK3 Biology Open. doi: 10.1242/bio.20136692. PMID: 24429107

Tuxworth R.I., Chen H., Vivancos V., Carvajal N., Huang X., and Tear G. (2011). The Batten disease gene CLN3 is required for the response to oxidative stress. Hum. Mol. Genet. 20, 2037-47. PMID: 21372148

Tuxworth R.I., Vivancos V., O’Hare M.B. and Tear G. (2009). Interactions between the juvenile Batten disease gene, CLN3, and the Notch and JNK signalling pathways. Hum. Mol. Genet. 18, 667-78. PMID: 19028667

View all publications in research portal