(HealthDay News) — A novel gene has been identified as having a regulatory role in nerve conduction velocity, according to an experimental study published online August 12 in The Journal of Pathology.

Using a classical genetic approach, Susanne Lemcke, PhD, from the University of Lübeck in Germany, and colleagues examined novel genes controlling nerve conduction.

The researchers identified EAE31, a locus controlling latency of motor evoked potentials (MEPs) and clinical onset of experimental autoimmune encephalomyelitis, using quantitative trait mapping in F2 progeny of B10/SJL mice. The quantitative trait gene for EAE31 was identified as inositol polyphosphate-4-phosphatase type II (Inpp4b), using a combination of congenic mapping, in silico haplotype analyses, and comparative genomics. Among different mouse strains, sequence variants of Inpp4b were identified, and these correlated with differences in individual cortical MEP latency. Transgenic mice carrying the longer-latency allele (Inpp4b474R/548P) in the C57BL/6J background exhibited significantly longer cortical MEP latencies. In German and Spanish multiple sclerosis cohorts, an association of an INPP4B polymorphism (rs13102150) was observed with multiple sclerosis.

“This study reports an interesting observation, but the neurobiological mechanisms, which provide a clear picture of why INPP4B impairs conduction velocity remain unclear,” writes Hans Lassmann, M.D., from the Medical University of Vienna, in an accompanying editorial.

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