No influence of KIF1B on neurodegenerative markers in multiple sclerosis

Abstract

In search of genetic causes of multiple sclerosis (MS), a number of genes have consistently shown association with MS susceptibility in the past couple of years.1 All of these identified genes are directly or indirectly involved with the inflammatory process. However, it has become increasingly clear that MS consists of both an inflammatory and a progressive neurodegenerative process,2 which is illustrated by the fact that new and potent anti-inflammatory drugs have been unable to halt neurodegeneration. The relation between episodes of inflammation and the neurodegenerative component characterized by irreversible axonal loss are far from clear at this point. Some authors have argued that neurodegeneration is independent of inflammation, while others argue that the 2 components are closely associated and are actually interdependent.2,3 The neurodegenerative component is clinically highly relevant since it is held predominantly responsible for disability accumulation, although several questions regarding this issue remain.2 Until recently, no genetic marker for neurodegeneration in MS was identified. However, in 2008, it was reported for the first time that a “neurodegenerative gene,” i.e., the KIF1B rs10492972 [C] variant, was associated with MS susceptibility.4 KIF1B is involved in axonal transport of mitochondria and synaptic vesicle precursors. Dysregulation of axonal transport plays a role in several neurodegenerative diseases.4 The authors suggested that KIF1B could be the first gene involved in MS susceptibility with a possible neurodegenerative effect.4 Unfortunately, this finding could later not be confirmed in other …