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Geoff Woods

Understanding Mendelian disorders of neurodevelopment

Our research derives from patients with Mendelian disorders of neurodevelopment. The results are of use to the families and their clinicians, and define essential genes and processes in human neurodevelopment.

Our studies are primarily translational:

  • We ascertain, study and classify people/families with genetic diseases through specialist clinics and extensive collaboration.
  • We discover the causative genes for the phenotypes associated with these diseases by characterizing potential pathogenic mutations.
  • We perform whatever further studies are needed to prove mutations are pathogenic, define the function of the gene in normal development, and determine how mutation leads to disease phenotypes.
  • Finally, we offer clinical support and molecular genetic diagnosis through the NHS East Anglian Genetics Service.

Our current main focus is Mendelian disorders of painlessness and of excess pain, ascertained from Paediatric and Adult Neurology, Rheumatology, Pain clinics and my clinical work.  We are part of a CamPain network of Cambridge physicians and scientists seeking to understand painful disorders and produce better treatments. Together we are developing methods to assess nociceptor spinal cord and central nervous system responses in pain disorders, with our team's contribution being to identify and investigate potential underlying driver genetic changes. We also study painlessness which can be classified as: failures of the pain-sensing nervous system to develop; inability of pain-sensing neurons to respond to nociceptive stimuli; or neuropathies that uniquely or particularly affect peripheral nociceptors. We work on new disorders in each category. For example, in collaboration with Professor Vallier in the Stem Cell Centre and MedImmune, we are investigating the 'créer' events that allow a mitotically active neural crest progenitor to change into a post-mitotic nociceptor. The genes regulating these developmental steps, such as TRKA and NGF, will have other essential post-natal roles in pain — and hence are candidates to generate novel analgesics.


Woods lab

Key papers:

Chen YC et al. Transcriptional regulator PRDM12 is essential for human pain perception. Nature Genet. 47, 803–808 (2015).

Nahorski MS, Al-Gazali L, Hertecant J, Owen DJ, Borner GH, Chen YC, Benn CL, Carvalho OP, Shaikh SS, Phelan A, Robinson MS, Royle SJ & Geoffrey Woods C. A novel disorder reveals clathrin heavy chain-22 is essential for human pain and touch development. Brain 138, 2147–2160 (2015).

Woods CG* & Bennett D*. Painful and painless channelopathies – invited review. Lancet Neurol. 13, 587–599 (2014). *corresponding authors.

Woods CG & Parker A. Investigating microcephaly. Arch Dis Child. 98, 707–713 (2013).

Weiss, J., Pyrski, M., Jacobi, E., Bufe, B., Willnecker, V., Schick, B., Zizzari, P., Gossage, S.J., Greer, C.A., Leinders-Zufall, T., Woods, C.G., Wood, J.N. and Zufall, F. Loss-of-function mutations in sodium channel Nav1.7 cause anosmia. Nature 472, 186–190 (2011).

Sir, J.H., Barr, A.R., Nicholas, A.K., Carvalho, O.P., Khurshid, M., Sossick, A., Reichelt, S., D'Santos, C., Woods, C.G.* and Gergely, F.* A primary microcephaly protein complex forms a ring around parental centrioles. Nature Genet. 43, 1147–1153 (2011). * corresponding authors.

Cox, J.J., Willatt, L., Homfray, T. and Woods, C.G. A SOX9 duplication and familial 46,XX developmental testicular disorder. N. Engl. J. Med. 364, 91–93 (2011).

Cox, J. J., Sheynin, J., Shorer, Z., Reimann, F., Nicholas, A. K., Zubovic, L., Baralle, M., Wraige, E., Manor, E., Levy, J., Woods, C. G. and Parvari, R. Congenital insensitivity to pain: novel SCN9A missense and in-frame deletion mutations. Hum. Mutat. 31, E1670–1686 (2010).

Reimann, F., Cox, J. J., Belfer, I., Diatchenko, L., Zaykin, D. V., McHale, D. P., Drenth, J. P., Dai, F., Wheeler, J., Sanders, F., Wood, L., Wu, T. X., Karppinen, J., Nikolajsen, L., Männikkö, M., Max, M. B., Kiselycznyk. C., Poddar, M., Te Morsche, R. H., Smith, S., Gibson, D., Kelempisioti, A., Maixner, W., Gribble, F. M. and Woods. C. G. Pain perception is altered by a nucleotide polymorphism in SCN9A. Proc. Natl Acad. Sci. USA 107, 5148–5153 (2010).

Jacoby, M., Cox, J. J., Gayral, S., Hampshire, D. J., Ayub, M., Blockmans, M., Pernot, E., Kisseleva, M. V., Compère, P., Schiffmann, S. N., Gergely, F., Riley, J. H., Pérez-Morga, D., Schurmans, S. and Woods, C. G. INPP5E mutations cause primary cilium signaling defects, ciliary instability and ciliopathies in human and mouse. Nature Genet. 41, 1027–1031 (2009).

Cox, J., Reimann, F., Nicholas, A. K., Thornton, G., Roberts, E., Springell, K., Karbani, G., Jafri, H., Mannan, J., Raashid, Y., Al-Gazali, L., Hamamy, H., Valente, E. M., Gorman, S., Williams, R., McHale, D. P., Wood, J. N., Gribble, F. and Woods, C. G. SCN9A channelopathy cause a congenital inability to experience pain. Nature 444, 894–898 (2006).

Professor Geoff Woods

Personal Chair

Department: Medical Genetics


01223 767811


Plain English

Mendelian disorders are inherited in families in a particular pattern that reflects the inheritance of a single mutated gene on one or both copies of the chromosome. There are more than 5000 such disorders in humans, and detailed understanding of the underlying gene changes is needed. By determining the DNA codes of family groups with new disorders, it can be possible to find the gene mutation that is responsible for that disease. We are currently focusing on the inherited disorders that result in the inability to feel pain or conversely excess pain. Our work has found the genes that are responsible for some of these disorders, and our hope is that these findings may contribute to the development of new painkillers.

Group members

Michael Nahorski · Ya-Chun (Alva) Chen · Samiha Shaikh


Medical Research Council

Cambridge NIHR Biomedical Research Centre

Addenbrooke's Charitable Trust