Handbook of Neurochemistry and Molecular Neurobiology: Brain and Spinal Cord Trauma (Springer Reference)

685 Pages·2009·11.95 MB·English

by  Naren L. Banik

Handbook of Neurochemistry and Molecular Neurobiology
BrainandSpinalCordTrauma
Abel Lajtha (Ed.)
Handbook of
Neurochemistry and
Molecular Neurobiology
Brain and Spinal Cord Trauma
Volume Editors: Naren Banik and Swapan K. Ray
With120 Figures and28Tables
Editor
AbelLajtha
Director
CenterforNeurochemistry
NathanS.KlineInstituteforPsychiatricResearch
140OldOrangeburgRoad
Orangeburg
NewYork,10962
USA
VolumeEditors
NarenBanik SwapanK.Ray
DepartmentofNeurosciences DepartmentofPathology,Microbiologyand
DivisionofNeurology Immunology
MedicalUniversityofSouthCarolina UniversityofSouthCarolinaSchoolofMedicine
96JonathanLucasStreet,Suite309 6439GarnersFerryRoad
Charleston,SC29425 Building2,RoomC11
USA Columbia,SC29209
USA
LibraryofCongressControlNumber:2006922553
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Preface
Thisvolumedealswithnervoussysteminjuries,repairandtherapeuticapproaches,andsomeneurodegen-
erative diseases not covered in other volumes of the Handbook. How current research changed our
understandingoftheepidemiology,pathophysiologicalmechanisms,celldemiseleadingtolossoffunction,
whether in traumatic brain injury (TBI), spinal cord injury (SCI), or neurodegenerative diseases, and
therapeuticapproachestoamelioratedysfunctionofthesedevastatingconditionsareemphasized.Central
nervoussystem(CNS)trauma(TBIandSCIcombined)isoneofthemajorcausesofdeathintheUnited
Statesandisoneofthemainkillers(perhapsnumberone)oftheyoungpeoplebelowthemid-thirties.While
TBIkillsthemajorityofthesevictims,SCI,dependingontheseverity,leadstolifelongdisabilityanddespair
atthetimeoftheirhighestproductivity.Oneofthemostimportantareasinmedicinenowistherepairofthe
damagedtissueofinjuredbrainandspinalcordsothefunctionmaybeimprovedorrestored.Themajor
problemfacingcliniciansandresearchersisthefailureofbrainandspinalcordtorepairorregeneratethe
damagedareas,perhapsbecausetheseorgansaresooverlycomplex,functionallyandstructurally,containing
differentcelltypes,fiberpathways,messengers(neurochemicals),andotherelements.Inaddition,damage
totissueintraumaiscausedbynotone,butmanymulti-destructivepathways.
Inspiteofthiscomplexity,neurosciencehasmadesignificantadvancesinunderstandingofthedelayed
injuryprocess(i.e.secondarydamage),providingopportunitiesfortarget-basedtherapeuticintervention,
improved imaging, blood vessel growth, regeneration, and tissue transplantation, including stem cell
application.Duringthelasttwodecadesofvigorousresearch,scientistshaveidentifiedseveralsecondary
injuryfactors,althoughmanystillremainunknown,thatdamageordestroyinjuredbrainandspinalcord.
Theyaretryingtounderstandhowthesefactors,includingincreasedcalciumandcalcium-mediatedevents
(namely lipases and proteases), free radicals, excitotoxicity, alterations in structural integrity of cell
membrane, axonaldamageinwhitematter,and reduction inbloodflow,leadtoapoptosis andnecrosis
of neurons and myelinating oligodendrocytes and ultimately destruction of tissue following injury.
Althoughbetterimagingandpharmacologicaltherapyusingmethylprednisoloneandsurgicalmanipula-
tion,particularlyinSCI,haveslightlyimprovedtheclinicalmanagementofpatients,wearestillnowhere
near acknowledging any realrecoveryof function. Yes, advanceshave been made over the years.Yet, we
knowlittleandmuchneedstobelearnedabouthowtoreducedisabilityandrestorefunctioninTBIand
SCI. Therefore, vigorous research is needed in other areas, including regeneration, protection of cells
andpreservation ofaxons, imaging bydistension tensorimaging (DTI)andrestoring bloodsupply that
mayhelpfurther improvefunction following TBIand SCI. Some of these detrimental pathwaysmay be
commontoneurodegenerativediseasesuchasAlzheimer’sdisease(AD),Parkinson’sdisease(PD),multiple
sclerosis(MS),andamyotrophiclateralsclerosis(ALS),whichwillalsobenefitfromthisresearchattenuat-
ingdysfunction.
The chapters included in this volume clearly demonstrate the progress made in understanding the
destructive mechanisms involved not only in TBI and SCI, but also in other neurodegenerative and
neoplasticdiseases.Theworkonenzymes(proteasesandlipases),lipids,proteins,freeradicals,andothers
haveestablishedrolesassignificantmediatorsofcelldamageanddisintegrationofmembranearchitecture
indiseasesandinjuries.Wecanlearnmoreabouthowtheblood-brainbarrier(BBB)orspinalcord-blood
barrieraremaintainedsothatforeignelementscannotenterandprovideprotection,howelementsenter
theCNSthroughthebarrierthathasbeencompromisedininjuryandinflammatorydiseases(e.g.MS,AD,
PD), and how to kill brain tumor cells by increasing the permeability. The contributors in this volume
discussedtheimportanceofmicrocirculationintermsofbloodflowthroughmicrovesselgrowthfollowing
vi Preface
injury or in ischemic conditions, controlling angiogenesis in CNS tumor, and maintaining the BBB
function. Other chapters have described cell death and degenerative processes in macular degeneration
and diabetic retinopathy as well as in autoimmune diseases likeoptic neuritis and experimental allergic
encephalomyelitis(EAE),whichistheanimalmodelofMS.Severalchaptershaveelaboratedondiseases,
includingadrenoleukodystorphy(asecondarydemyelinatingdisease),peripheralneuropathy,andhyper-
ammonemia.Atthecellularlevel,whitematterdegeneration,includingaxonandcelldeathinCNSinjuries
aswellasinneurodegenerativedisease,hasbeenemphasized.AlthoughthereislittleornoCNSrepairor
regeneration in the brain, a chapter has been devoted to elucidate the potential therapeutic aspects of
utilizingstemcelltransplantation.Finally,chaptershavebeenincludedontherehabilitationofSCIpatients
andcurrentmanagementandongoingclinicaltrialsfortreatment.Thestudiesdescribedinthesechapters
have also emphasized the importance of therapeutic strategies to combat dysfunction in injuries and
diseases.
OurknowledgeofthepathophysiologyofCNSinjuriesanddiseaseshasincreasedovertheyearsonly
duetothetremendousadvancesthathavebeenmadeinmanyareasofbasicneuroscienceresearch.The
excitingfindingsofallcontributorstothisvolumeemphasizeonemostimportantaspect–applyingbasic
neurosciencetotheunderstandingofclinicalproblemsofpatientswithdiseasesandinjuries.Needlessto
say, althoughwe have made substantial progress in some areas,further research is vital in areassuch as
regeneration/repair, axonal guidance, preservation and protection of cells and their processes, genetic
regulation,growthfactors,transplantation,andstemcellbiologyforattenuationofdysfunctionthrough
developmentofnewtherapeuticstrategies.Theadvancesmadethusfaronscientificresearchgiveus,the
researchers,hopethatfurtherprogresswillhelprestorefunctionandcureCNSdiseasesinthefuture.
We thank our authors for their excellent contributions to this volume. We also thank Ms. Denise
Matzelle and Ms. Kristine Immediato for their patience and efforts in making this volume into its
finalform.
NarenL.BanikandSwapanK.Ray
Table of Contents
Preface .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. .. v
Contributors.. . .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. . xi
1 BrainTumorAngiogenesis .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. .. 1
S.Lakka.J.S.Rao
2 Adrenoleukodystrophy:Molecular,Metabolic,Pathologic,and
TherapeuticAspects .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. . 13
M.A.Contreras.I.Singh
3 Hyperammonemia.. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. . 43
V.Felipo
4 GlutamateandCytokine‐MediatedAlterationsofPhospholipidsin
HeadInjuryandSpinalCordTrauma . .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. . 71
A.A.Farooqui.L.A.Horrocks
5 KynureninesintheBrain:PreclinicalandClinicalStudies,Therapeutic
Considerations .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. . 91
C.Kiss.L.Ve´csei
6 NeurofibromatosisTypeI:FromGeneticMutationto
TumorFormation .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 107
S.L.Thomas.G.H.DeVries
7 AmyloidandNeurodegeneration:Alzheimer’sDiseaseand
RetinalDegeneration . . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 131
A.Prakasam.C.Venugopal.A.Suram.J.Pacheco‐Quinto.Y.Zhou.
M.A.Pappolla.K.A.Sharpe.D.K.Lahiri.N.H.Greig.B.Rohrer.
K.Sambamurti
8 DiabeticRetinopathy.. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 165
E.Bowie.C.E.Crosson
9 NeurotransmittersandElectrophysiologyinTraumaticBrainInjury .. . .. .. 179
C.E.Dixon.A.E.Kline
#2009SpringerScienceþBusinessMedia,LLC.
viii Tableofcontents
10 FreeRadicalsandNeuroprotectioninTraumaticBrainand
SpinalCordInjury .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 203
E.D.Hall
11 NeuroimmunologyofParaproteinemicNeuropathies .. .. .. . .. .. .. . .. .. 229
A.A.Ilyas
12 ProteolyticMechanismsofCellDeathintheCentralNervousSystem. . .. .. 249
S.F.Larner.R.L.Hayes.K.K.W.Wang
13 NitricOxideinExperimentalAllergicEncephalomyelitis .. .. . .. .. .. . .. .. 281
S.Brahmachari.K.Pahan
14 TheBlood–BrainBarrier—Biology,Development,andBrainInjury . .. . .. .. 303
C.L.Keogh.K.R.Francis.V.R.Whitaker.L.Wei
15 PhospholipaseA inCNSDisorders:ImplicationonTraumatic
2
SpinalCordandBrainInjuries . . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 321
N.-K.Liu.W. Titsworth.X.-M.Xu
16 AxonalDamageduetoTraumaticBrainInjury. .. . .. .. .. .. . .. .. .. . .. .. 343
K.E.Saatman.G.Serbest.M.F.Burkhardt
17 Blood–CentralNervousSystemBarriers:TheGatewayto
Neurodegeneration,NeuroprotectionandNeuroregeneration .. .. .. . .. .. 363
H.S.Sharma
18 EngineeredAntibodyFragmentsasPotentialTherapeuticsagainst
MisfoldedProteinsinNeurodegenerativeDiseases .. .. .. .. . .. .. .. . .. .. 459
E.Kvam.A.Messer
19 PathogenesisandTreatmentofHIV-associatedDementia:RecentStudies
inaSCIDMouseModel . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 471
W.R.Tyor
20 StemCellTransplantationTherapyforNeurologicalDiseases . .. .. .. . .. .. 491
X.‐Y.Hu.J.‐A.Wang.K.Francis.M.E.Ogle.L.Wei.S.P.Yu
21 Ubiquitin/ProteasomeandAutophagy/LysosomePathways:Comparison
andRoleinNeurodegeneration . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 513
N.Myeku.M.E.Figueiredo-Pereira
22 ExperimentalAutoimmuneEncephalomyelitisinthePathogenesisof
OpticNeuritis:IsCalpainInvolved? .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 525
M.K.Guyton.A.W.Smith.S.K.Ray.N.L.Banik
23 ProteinCarbonylationinNeurodegenerativeandDemyelinating
CNSDiseases . . .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 543
O.A.Bizzozero
Tableofcontents ix
24 ClinicalConsiderationsinTranslationalResearchwithChronicSpinalCord
Injury:InterventionReadinessandInterventionImpact .. .. . .. .. .. . .. .. 563
J.S.Krause.S.D.Newman.S.S.Brotherton
25 EstrogenasaPromisingMulti-ActiveAgentfortheTreatmentof
SpinalCordInjury .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 581
E.A.Sribnick.D.D.Matzelle.S.K.Ray .N.L.Banik
26 ImmunotherapyStrategiesforLewyBodyandParkinson’sDiseases . . .. .. 599
L.Crews.B.Spencer.E.Masliah
27 ClinicalOutcomesAfterSpinalCordInjury.. .. .. . .. .. .. .. . .. .. .. . .. .. 615
J.S.Krause.S.D.Newman
28 SpinalCordInjury–AClinicalPerspective .. .. .. . .. .. .. .. . .. .. .. . .. .. 633
A.Varma
29 CubingtheBrain:MappingExpressionPatternsGenome-Wide.. .. .. . .. .. 649
M.H.Chin.D.J.Smith
Index . .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. . .. .. .. .. . .. .. .. . .. .. 657