While the majority of scientists dedicated to multiple sclerosis research focus on genetic regulators of conditions such as autoimmunity, demyelination, inflammation, and neurodegeneration, a team from the University of Lubeck in Germany, led by Saleh M. Ibrahim, MD, PhD, focuses on genetic regulators of conduction velocity. The team is uncovering how certain genetic alterations aggravate disease in multiple sclerosis patients and mice with multiple sclerosis-like experimental autoimmune encephalomyelitis (EAE).
“Impairment of nerve conduction is a common feature in neurodegenerative and neuroinflammatory diseases such as multiple sclerosis,” stated Dr. Ibrahim, as reported by a press release from the publishing organization Elsevier. “Measurement of evoked potentials (whether visual, motor, or sensory) is widely used for diagnosis and recently also as a prognostic marker for multiple sclerosis.”
The gene culprit identified by Dr. Ibrahim’s group is the inositol polyphosphate-4-phosphatase, type II (INPP4b) gene. As detailed in the team’s article published in The American Journal of Pathology, “Nerve Conduction Velocity is Regulated by the Inositol Polyphosphate-4-Phosphatase II Gene,” polymorphisms, or two variants of the same gene, of Inpp4b produce different speeds of nerve conduction in multiple sclerosis patients and mice with EAE.
Dr. Ibrahim and colleagues made their discovery through several genomic approaches, including quantitative trait mapping, congenic mapping, in silico haplotype analyses, comparative genomics, and transgenic mice. After identifying Inpp4b as the gene behind the genetic locus EAE31, which was previously shown to control motor evoked potential latency and clinical onset of mouse EAE, the team analyzed the region in 8 mice strains.
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