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In a paper published today in the journal Scientific Reports, a pair of researchers at the University of California, San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences report that inhibiting the ability of immune cells to use fatty acids as fuel measurably slows disease progression in a mouse model of multiple sclerosis (MS).
MS is an autoimmune disease resulting from damage to the myelin sheath, a protective layer surrounding nerve cells. When the sheath is damaged, nerve impulses are slowed or halted, resulting in progressive physical and neurological disabilities. The cause of the damage is inflammation occurring when the body’s immune cells attack the central nervous system (CNS).
Nerve cell with protective layers of myelin.
Currently, no approved drug or therapy for MS targets fatty acid metabolism. And the specificity of the target – inhibiting a single enzyme – suggests that adverse side effects associated with existing treatments, such as increased infection risk, is unlikely.
“We expect that because immune cells not in lesions in the CNS are able to use available glucose, they will function just fine during infection and that inhibition of this pathway would not produce general immune suppression,” Shriver said.
The enzyme-inhibitor used by Manchester and Shriver in their study is a drug already tested in humans with congestive heart failure, and was generally well-tolerated. The scientists are now using mass spectrometry to determine whether their results in the mouse model are translatable to humans. “We are interested in determining how this pathway is utilized in human tissue samples from MS patients,” Manchester said.
Funding for this study came from the National Institutes of Health and the National Institute of Neurological Disorders and Stroke.
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