Dr Richard Tuxworth MA PhD

Dr Richard Tuxworth

Institute of Cancer and Genomic Sciences
Lecturer in Molecular Genetics

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 a lecturer in the Institute of Cancer and Genomic Sciences. He is a cell biologist with a particular interest in lysosomal function in the nervous system and understanding why lysosomal dysfunction contributes to neurodegenerative 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 October 2012 in the School of Clinical and Experimental Medicine.


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
  • 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 on the contact details above, or for any general doctoral research enquiries, please email dr@contacts.bham.ac.uk or call +44 (0)121 414 5005.


Richard Tuxworth is a cell biologist interested in disorders of the nervous system. He studies both early-onset inherited forms of neurodegeneration caused by lysosomal dysfunction and aspects of the common neurodegenerative disorders associated with old age.

Lysosomal storage disorders and neural development

Lysosomes are low-pH organelles critical for recycling in cells and for coordination of growth and stress signaling. 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 because the flies can be rapidly manipulated genetically to mirror some of the changes seen in the human lysosomal storage disorders.

These models are then used to ask what happens to neural development when lysosomal function is impaired and to assess the consequences for nervous system function. This approach combines genetics, cell biology, neurobiology and imaging with cell-based studies and proteomics.

The cell biology of neurodegeneration

Common late-onset neurodegenerative disorders such as Alzheimer’s disease are an increasing burden on the health services and more generally society as the population ages. There are no currently effective methods of slowing disease progression. Richard and colleagues in the College of Medical and Dental Sciences are investigating novel methods of intervening in neurodegenerative disorders to relieve disease burden. Richard’s group uses simple models of neurodegenerative disease developed in fruit flies to perform rapid surveys of potential new methods of intervention. Successful methods can then be validated in other systems.


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