Childhood trauma could affect the trajectory of multiple sclerosis development and response to treatment in adulthood, a new study suggests. Multiple sclerosis is a progressive autoimmune disease in which the body attacks and strips away the protective coating around neurons, resulting in a wide range of neurological symptoms.

In a mice-based study, researchers found that mice that had experienced stress when young were more likely to develop the autoimmune disorder and less likely to respond to a common treatment.

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"Mice that had early-life trauma were more susceptible to experimental autoimmune encephalomyelitis (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," said researcher Yee Ming Khaw from the University of Illinois at Urbana-Champaign in the US.

In the study, published in the journal Nature Communications, the team studied a mouse model of multiple sclerosis. The mice were genetically susceptible to experimental autoimmune encephalomyelitis, the model most widely used for studying MS.

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

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The researchers traced the EAE triggers to the immune system — in particular, a receptor on immune cells that binds to the stress hormone norepinephrine. The researchers found that childhood stress in the mice triggered a prolonged release of norepinephrine. The receptor was activated for long periods of time, which led the cells to decrease their expression – leaving the immune system less equipped to respond to the stress and inflammation of EAE.

Importantly, mice that developed EAE after stress in their childhood trauma did not respond to treatment with interferon beta, one of the initial therapies most widely prescribed to individuals with multiple sclerosis. (IANS)