ROCHESTER, N.Y., Jan. 27 (UPI) — Scientists found the over-active immune response that characterizes multiple sclerosis causes synapses in the brain to get overloaded and stop functioning, resulting in the cognitive declines many patients see later in life, according to a new study.

The research confirms a new understanding of what patients say is the most frustrating part of the disease, and may help scientists find ways to treat an aspect of MS not helped by current immunosuppressive drugs.

MS is characterized by the immune system attacking myelin, the fatty white matter tissue in the central nervous system that protects the connections between nerve cells. If myelin is lost or damaged, signals between the cells can be delayed, disrupted or blocked.

As many as 70 percent of MS patients also develop cognitive decline, but there are no ways to treat or prevent it and. While previous studies have shown there was a chance neurons outside areas of the brain involved in movement were damaged by the disease, scientists said they were not sure until the new findings.

“For too long, MS has been characterized as a disease that impairs people’s mobility, speech, or vision,” said Dr. Harris Gelbard, director of the Center for Neural Development and Disease at the University of Rochester, in a press release. “However, the aspect of the disease that many patients complain has the greatest impact on their quality of life is the loss of cognitive independence.”

For the study, published in the Journal of Neuroscience, scientists conducted experiments with mice showing neurons in the hippocampus, which is not involved with motor control, were damaged at the synapse, the point where neurons meet to exchange chemical signals.

The scientists found distress signals sent throughout the brain because of the over-activated immune system influence microglia — which normally help keep synapses healthy — to switch to a more aggressive role. Part of this is the release of platelet-activating factor, or PAF. High levels of PAF over-activate signals between neurons, which scientists compared to a power surge that destroys the receiving end of the synapse as part of a repeating, chronic and self-perpetuating cycle.

Research is needed to find drugs that may suppress the overreaction in the brain, including the consideration of a drug being tested for HIV-associated neurological conditions, the scientists said.

“This study identifies for the first time a new disease mechanism in MS which causes damage to neurons independent of the loss of white matter and demyelination that is the hallmark of the disease,” said Dr. Matthew Bellizzi, a neurologist and researcher at the University of Rochester Medical Center. “This damage represents another component of the disease and one that is not prevented by the current immunosuppressive drugs employed to treat MS.”

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