Bridgingthegap:axonalfusiondrivesrapidfunctionalrecoveryofthenervoussystem

摘要： Injuriestothecentralorperipheralnervoussystemfrequentlycauselong-termdisabilitiesbecausedamagedneuronsareunabletoefficientlyself-repair.Thisinherentdeficiencynecessitatestheneedfornewtreatmentoptionsaimedatrestoringlostfunctiontopatients.Comparedtohumans,anumberofspeciespossessfargreaterregenerativecapabilities,andcanthereforeprovideimportantinsightsintohowourownnervoussystemscanberepaired.Inparticular,severalinvertebratespecieshavebeenshowntorapidlyinitiateregenerationpost-injury,allowingseparatedaxonsegmentstore-join.Thisprocess,knownasaxonalfusion,representsahighlyefficientrepairmechanismasaregrowingaxonneedstoonlybridgethesiteofdamageandfusewithitsseparatedcounterpartinordertore-establishitsoriginalstructure.OurrecentfindingsinthenematodeCaenorhabditiseleganshaveexpandedthepromiseofaxonalfusionbydemonstratingthatitcanrestorecompletefunctiontodamagedneurons.Moreover,werevealedtheimportanceofinjury-inducedchangesinthecompositionoftheaxonalmembraneformediatingaxonalfusion,anddiscoveredthatthelevelofaxonalfusioncanbeenhancedbypromotinganeuronsintrinsicgrowthpotential.Acompleteunderstandingofthemolecularmechanismscontrollingaxonalfusionmaypermitsimilarapproachestobeappliedinaclinicalsetting. ... （共4页）