#ECTRIMS2018 – Researcher Presents Data About Myelocortical MS, a New Disease Subtype

#ECTRIMS2018 – Researcher Presents Data About Myelocortical MS, a New Disease Subtype
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A new subtype of multiple sclerosis (MS) — called myelocortical MS (MCMS) — is characterized by cortical neuronal loss, but not by loss of myelin in the brain’s white matter, according to a study.

Research on this new type of MS was presented today at the 34th congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), in a presentation titled “Myelocortical multiple sclerosis: cortical neuronal loss in the absence of cerebral white matter demyelination.” ECTRIMS is being held in Berlin, Germany, today-Friday (Oct. 10-12).

The presenter was Bruce Trapp, PhD, chairman of the department of Neurosciences at the Cleveland Clinic’s Lerner Research Institute.

Loss of myelin — the protective layer of nerve fibers — is regarded as the driver of neuronal degeneration and permanent neurological disability in MS. White matter, which is made of nerve fibers and makes up about half of the human brain, is the main target for immune system attacks in these patients.

However, studies using magnetic resonance imaging (MRI) have indicated that myelin loss and neuronal degeneration can occur independently.

Aiming to explore this further, researchers assessed if MS brains showed signs of neuronal loss in the cerebral cortex — a gray matter part of the brain involved in diverse functions, including memory, information processing, and motor control — independent of demyelination in the brain’s white matter.

Brains and spinal cords were removed at autopsy from MS patients. Of 97 brain samples analyzed, 12 had no signs of cerebral white matter demyelination.

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These 12 cases were compared to 12 other MS cases with white matter lesions, namely in the cerebral white matter, cortex, and in the spinal cord. The team compared atrophy (shrinkage,  an MS feature), MRI measures, and number of neurons between both MS groups, and investigated possible correlations between alterations in MRI and disease processes.

Results showed that cases without cerebral macroscopic (visible with the naked eye) lesions had myelin loss in the spinal cord and cortex, but no brain white matter demyelination.

However, these brains showed significantly greater cortical neuronal loss, cortical thinning, and MRI abnormalities in cerebral white matter, compared to brains from healthy controls. These features were similar to those seen in MS brains with cerebral white matter demyelination. This suggests that cortical neuronal loss is independent from white matter demyelination in patients with MCMS, the researchers noted.

Also, the 12 brains without cerebral white matter myelin loss showed swollen myelinated nerve fibers —  previously associated with central nervous system degeneration — in white matter areas with MRI abnormalities.

“A subtype of MS, which we call myelocortical multiple sclerosis (MCMS), is characterized by demyelination of spinal cord and cerebral cortex, but not of cerebral white matter. Cortical neuronal loss is not accompanied by cerebral white-matter demyelination and is therefore an independent pathological event in MCMS,” the researchers wrote.

Trapp also is the first author of a recent study describing MCMS.

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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