Professor of Neuroscience
Matthew Wood graduated in Medicine from the University of Cape Town in 1987, working in clinical Neuroscience before gaining a doctorate in Physiological Sciences from the University of Oxford in 1993. He is currently University Lecturer, and Fellow and Tutor in Medicine and Physiology at Somerville College.
Matthew’s research is in field of gene therapy for degenerative disorders of the nervous system and muscle. The main focus is the investigation of novel therapeutic approaches utilising short nucleic acids to target messenger RNA. Targeting RNA has the potential to allow modification of the target transcript, reprogramming of endogenous genetic defects or the targeting of specific disease alleles, all the while maintaining endogenous regulation of the target gene. Current work is investigating the potential of single-stranded antisense oligonucleotides for the modification of mRNA splicing, for example in Duchenne muscular dystrophy. In addition, the potential of double-stranded RNA for gene silencing, known as RNA interference (RNAi), is being investigated for the silencing of target genes and mutant alleles both in muscle and in the nervous system. In particular, RNAi has great potential as a future therapeutic agent for currently untreatable neurodegenerative disorders such as Parkinson’s disease.
Delivery of siRNA to the mouse brain by systemic injection of targeted exosomes.
Alvarez-Erviti L. et al, (2011), Nat Biotechnol, 29, 341 - 345
A modular RNA delivery system comprising spherical nucleic acids built on endosome-escaping polymeric nanoparticles
Garcia-Guerra A. et al, (2023), Nanoscale Advances
Non-uniform dystrophin re-expression after CRISPR-mediated exon excision in the dystrophin/utrophin double-knockout mouse model of DMD.
Hanson B. et al, (2022), Mol Ther Nucleic Acids, 30, 379 - 397
RNase-H-mediated silencing in the CNS proves predictably nontrivial.
Moazami MP. and Wood MJA., (2022), Med (N Y), 3, 733 - 734
Antibody-oligonucleotide conjugate achieves central nervous system delivery in animal models for spinal muscular atrophy.
Hammond SM. et al, (2022), JCI Insight
High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer's Disease-Causing Mutations.
Sturchio A. et al, (2022), J Alzheimers Dis