简介:Traumaticinjuriestothecentralnervoussystem(CNS),includingtraumaticbraininjury(TBI)andspinalcordinjury(SCI),ofteninvolveanimmediatemechanicaldamagetoplasmamembranethatsurroundsneuronalsomataandaxons.Thisinitialdisruptionofplasmamembranefollowinginjurieshasbeenconvincinglydemonstratedbyincreasedmembrane
简介:Multiplesclerosisisachronicinflammatorydiseasethatisaccompaniedbydemyelinationandaxonaldamageresultinginneurologicaldeficits.Remyelinationisthenaturalendogenousrepairmechanismofdemyelinatedaxonsanditissupposedtoprotectaxons/neuronsfromdegenerationandthusthepatientfromprogressivedisability(FranklinandFfrench-Constant,2008).Currenttherapeuticsforpatientswithmultiplesclerosis
简介:Themanagementofneurologicaldisordershavehugeandincreasinghumanandeconomiccosts.Despitethis,thereisascarcityofeffectivetherapeutics,andthereisanextremeurgencyfornewandrealtreatments.Inthisshortreviewweanalyzesomepromisingadvancementsinthesearchofnewbioactivemoleculestargetingneuronalnitricoxidesynthase(nNOS),anenzymedeputedtothebiosynthesisofnitricoxide(NO).Indifferentconditionsofneuronaldamages,thismoleculeisoverproduced,contributingtothepathogenesisandprogressionofneuronaldiseases.TwomainapproachestomodulatenNOSarediscussed:afirstoneconsistinginthedirectinhibitionoftheenzymebymeansofsmallorganicmolecules,whichcanbealsoactiveagainstotherdifferenttargetsinvolvedinsuchdiseases.AsecondsectionisdedicatedtomoleculesabletopreventtheformationoftheternarycomplexN-methyl-D-aspartate(NMDA)-typeglutamatereceptors,postsynapticdensity-95(PSD95)protein-nNOS,whichisnecessarytoactivatethelatterforthebiosynthesisofNO.
简介:Brainischemicstrokeistheleadingcauseoflong-lastinginjury,disability,anddeathinadults.Althoughthebrainrepresentsonlyabout2%ofthetotalbodymass,itconsumesalmost20%ofthebody’soxygen.Asaresult,braincellsareextremelysensitivetohypoxia.Oncecerebralischemiaoccurs,thecoreofthe