Scientists find nerve damage may be reversible using organoid models
University of Cambridge researchers have developed miniature lab-grown brain and spinal cord systems that mimic human movement signal pathways. Using these organoids maintained for over a year, the team discovered that human neurons lose their ability to regrow damaged axons around day 150 of development, roughly corresponding to mid-pregnancy. The study, published in Cell Reports, identified a gene network that acts as a biological switch limiting axon growth as neurons mature. By blocking key regulators in this network, researchers were able to induce neurons to regain the ability to grow axons. Further work showed that an existing approved hormone drug, lynestrenol, significantly improved axon regrowth when tested on damaged neurons in the model. Senior author Dr. András Lakatos stated that the model provides evidence that the regeneration block happens during development and can still be reversed after that point. This single-source report comes from a University of Cambridge press release and has not been independently cross-referenced by No Spin Network.
What’s reported
Researchers at the University of Cambridge created miniature brain and spinal cord organoids that can send signals and trigger muscle contractions.
Axons from brain tissue grew across a gap to connect with spinal cord tissue, forming functional neural circuits.
Until about day 150 of development (roughly mid-pregnancy), damaged axons could still regrow; after that, regenerative ability sharply declined.
A network of genes was identified that limits axon growth as neurons mature and form synapses.
Blocking key regulators within that network allowed neurons to regrow axons again.
The hormone drug lynestrenol, approved for menstrual disorders and contraception, boosted axon regrowth when tested on damaged neurons.
The study was funded by UK Research and Innovation Medical Research Council and Spinal Research.
Open questions
Whether the strategy of targeting human neurons to regenerate axons will also help re-establish appropriate connections between brain and spinal cord cells in living patients. Additionally, whether lynestrenol itself is a viable candidate for spinal cord repair remains uncertain, as the lead author noted it “may not be the answer.”
Key figures
Dr. András Lakatos, senior author, Department of Clinical Neurosciences, University of Cambridge
George Gibbons, first author, Department of Clinical Neurosciences, University of Cambridge
Sources: ScienceDaily
