Early research in animal models and human samples reveals how loss of communication between nerve cells contributes to the symptoms of multiple sclerosis (MS), and shows how gene therapy could be used to preserve such connections and protect against vision loss.
Researchers say their work identifies a new approach for developing MS therapies that target nerve cell communication, rather than myelin loss, and could be applicable to other neurodegenerative disorders.
The study, “Targeted Complement Inhibition at Synapses Prevents Microglial Synaptic Engulfment and Synapse Loss in Demyelinating Disease,” was published in the journal Immunity.
MS is a neurological disease marked by inflammation and a self-attack of the immune system against a person’s brain, spinal cord, and optic nerves.
This attack damages the protective fatty substance covering nerve fibers (axons), which are necessary for proper transmission of nerve signals called myelin. As the myelin sheath is lost (demyelination), the communication between nerve cells is damaged or even interrupted, and nerve cell death occurs, leading to a range of disease symptoms.
Some MS patients experience a version of the disease called progressive MS, in which symptoms continuously worsen over time while their central nervous system (brain and spinal cord) shrinks (atrophies), and the junctions at which nerve cell terminals meet to communicate with each other, called synapses, are lost.
The majority of MS medications work to inhibit the self-attacking immune responses and inflammatory demyelination, but the neurodegenerative aspects of the disease have been more difficult to stop, particularly for patients with progressive MS.
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