Nerve damage is the main cause of disability in people with multiple sclerosis (MS), a disease
where the protective coating around nerves (called myelin) is lost. This problem also occurs in
other diseases affecting the brain, spinal cord, and peripheral nerves. It has been known that when
myelin is lost, nerve cells struggle to get enough energy, which is mainly supplied by tiny energy
factories inside the cells called mitochondria. Our team recently discovered that nerve cells can
respond to myelin loss by sending more mitochondria to the damaged areas to help keep the nerves
alive in a process we termed the axonal response of mitochondria to demyelination (ARMD).
Encouragingly, this response can be strengthened to protect nerves from damage.
In this project, we want to understand exactly how nerve cells control ARMD and how it changes
as people age or between males and females. We also want to learn how these changes affect the
quality and function of mitochondria in damaged and repaired nerves. To do this, we will study
mice that are specially modified to highlight damaged nerve cells and mitochondria, allowing us
to track and analyze them during myelin loss and repair. We will also study human patient samples
to confirm that our findings are relevant for people living with the disease.
By learning which cellular processes activate and tune ARMD and therefore protect nerves, we
hope to find new ways to slow or stop nerve damage in MS and related conditions, ultimately
helping to preserve movement, sensation, and quality of life for affected individuals.