title: Reduced axonal motor protein expression in non-lesional grey matter in multiple sclerosis.
abstract: Multiple sclerosis (MS) is a neurological disease characterised by central nervous system inflammation, demyelination, axonal degeneration and neuronal injury. Preventing neuronal and axon damage is of paramount importance in attempts to prevent disease progression. Intact axonal transport mechanisms are crucial to axonal integrity and evidence suggests these mechanisms are disrupted in MS. Anterograde axonal transport is mediated to a large extent through the kinesin superfamily proteins. Recently, certain kinesin superfamily proteins (KIF5A, KIF1B and KIF21B) were implicated in MS pathology.
  
  
  
  To investigate the expression of KIF5A, KIF21B and KIF1B in MS and control post-mortem grey matter.
  
  
  
  Using both quantitative real-time polymerase chain reaction (PCR) and Immunodot-blots assays, we analysed the expression of kinesin superfamily proteins in 27 MS cases and 13 control cases not linked to neurological disease.
  
  
  
  We have shown significant reductions in KIF5A, KIF21B and KIF1B messenger ribonucleic acid (mRNA) expression and also KIF5A protein expression in MS grey matter, as compared to control grey matter.
  
  
  
  We have shown significant reductions in mRNA and protein levels of axonal motor proteins in the grey matter of MS cases, which may have important implications for the pathogenesis of neuronal/axonal injury in the disease.
authors.affiliation: Multiple Sclerosis and Stem Cell Group, School of Clinical Sciences, University of Bristol, UK kelly.hares@bristol.ac.uk.
authors.forename: K
authors.initials: K
authors.lastname: Hares
authors.affiliation: Multiple Sclerosis and Stem Cell Group, School of Clinical Sciences, University of Bristol, UK.
authors.forename: K
authors.initials: K
authors.lastname: Kemp
authors.affiliation: Multiple Sclerosis and Stem Cell Group, School of Clinical Sciences, University of Bristol, UK.
authors.forename: C
authors.initials: C
authors.lastname: Rice
authors.affiliation: Multiple Sclerosis and Stem Cell Group, School of Clinical Sciences, University of Bristol, UK.
authors.forename: E
authors.initials: E
authors.lastname: Gray
authors.affiliation: Multiple Sclerosis and Stem Cell Group, School of Clinical Sciences, University of Bristol, UK.
authors.forename: N
authors.initials: N
authors.lastname: Scolding
authors.affiliation: Multiple Sclerosis and Stem Cell Group, School of Clinical Sciences, University of Bristol, UK.
authors.forename: A
authors.initials: A
authors.lastname: Wilkins
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D018450:Disease Progression; D015536:Down-Regulation; D005260:Female; D066128:Gray Matter / Q000737:chemistry* / Q000000981:diagnostic imaging; D006801:Humans; D016547:Kinesins / Q000032:analysis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000000981:diagnostic imaging / Q000235:genetics / Q000378:metabolism* / Q000401:mortality; D012333:RNA, Messenger / Q000235:genetics
chemical_list: C091053:KIF1B protein, human; C500506:KIF5A protein, human; D012333:RNA, Messenger; C523507:KIF2B protein, human; D016547:Kinesins
keywords: Axonal injury; KIF1B; KIF21B; KIF5A; axonal transport; grey matter; kinesin; multiple sclerosis; protein expression