The CNS white matter links billions of neurons in the grey matter. Its function depends on oligodendrocytes enwrapping neuronal axons with myelin to synchronize and increase information flow between neurons: essential for our cognitive abilities, our perception of the world and our motor skills. The importance of myelin becomes evident in diseases, such as multiple sclerosis, where myelin damage leads to cognitive and motor disability. Moreover, recent magnetic resonance imaging and genome-wide association studies have highlighted the contribution of myelin to many diseases that were previously considered ‘neuronal’ like dementia, schizophrenia, autism and bipolar disorder. However, unique to the CNS, myelin regeneration can occur spontaneously in demyelinating disease, as adult oligodendrocyte precursor cells (OPCs; a CNS stem cell that comprises 5% of all cells in the brain) respond to the demyelinating injury and differentiate into new myelinating oligodendrocytes. However, this process often fails, making OPCs differentiation an important therapeutic target.

We have previously shown that OPCs express neurotransmitter receptors and receive synaptic inputs from neuronal axons in the white matter, hence are capable of sensing changes in neuronal activity. The lab’s interest is to understand how signals from neurons induce OPCs to differentiate and myelinate axons during development and with normal ageing; this also could be an underlying mechanism for white matter plasticity.

The devastating consequences of dys/demyelination, in diseases like cerebral palsy, spinal cord injury and multiple sclerosis makes it important to study how OPCs differentiation is regulated. We are actively investigating how OPCs respond to myelin injury and whether neuronal activity and neurotransmitter signalling may regulate the myelin repair process. Our ultimate aim is to find new treatments for white matter disease.