Effect Of Childhood Trauma On Multiple Sclerosis

Childhood trauma can affect the course of development and response to treatment in young mice with multiple sclerosis.

The course of development of multiple sclerosis and response to treatment in can be influenced by childhood trauma.

The study conducted in mice showed that when young mice experienced stress they were more likely to develop the autoimmune disorder and were less likely to respond to a common treatment. However, treatment that activated an immune-cell receptor decreased the severity of the effects of childhood stress in the mice.

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‘Childhood trauma can affect the course of development and response to treatment in young mice with multiple sclerosis. Patients with childhood trauma may need different medical treatment.’
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The study conducted by researchers at the University of Illinois Urbana-Champaign is published in the journal Nature Communications.

Multiple sclerosis is a progressive autoimmune disorder in which the body’s immune system attacks and removes the protective coating around neurons that result in a wide range of neurological symptoms. Multiple sclerosis can occur due to both genetic and environmental factors.

Previous work had shown that early-life trauma can increase the risk of developing more severe multiple sclerosis but the researchers were not able to determine the exact mechanism for this. To study multiple sclerosis, the mice were genetically susceptible to experimental autoimmune encephalomyelitis (EAE).

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The development and progression of EAE in young mice that had been briefly separated from their mother and given a saline injection was compared with mice that had not experienced the same stress.

The first author of the study graduate student Yee Ming Khaw said, “Mice that had early-life trauma were more susceptible to EAE disease development and suffered prolonged motor paralysis with severe neuronal damage in the central nervous system, which we found was caused by a heightened immune response.”

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It was found that EAE activated the immune system, particularly the receptor on immune cells that binds to stress hormone norepinephrine. In mice, childhood stress triggered a prolonged release of norepinephrine. As the receptor was activated for a long duration, there was reduced expression of these cells. Hence, the immune system was less equipped to respond to the stress and inflammation of EAE.

One of the most widely prescribed first line therapies for multiple sclerosis is interferon beta. Mice that developed EAE after stress in their childhoods did not respond to treatment with interferon beta. On the other hand, the drug effectively prevented EAE progression in mice without childhood stress.

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In the further studies, the mice were given a compound that boosts the receptor's response. The treatment slowed damage to the spinal cord and also prevented paralysis. Even though they had not responded before, mice that received the treatment responded to interferon beta treatment.

Inoue said, “This work suggests that individuals with experience of childhood trauma develop autoimmune disease with symptoms and mechanisms that greatly differ from their peers with no history of childhood trauma, and may need different medical treatment. This receptor activator may be a therapeutic drug for MS patients with a history of childhood trauma.”

Future study plans to verify the mechanisms of the receptor and perform translational studies to confirm whether boosting the receptor in human patients with multiple sclerosis gives the same benefits as it did for the mice with EAE.

Inoue said, “We believe that the best approach to addressing autoimmune diseases in individuals with a history of childhood trauma or other risk factors is a comprehensive and personalized medicine approach that addresses the whole person.”

Source-Medindia