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Dementia: the Role of Alternative Therapies

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Dementia: the Role of Alternative Therapies Dementia:Dementia: TheThe RoleRole ofof AlternativeAlternative TherapiesTherapies MarwanMarwan SabbaghSabbagh MD,MD, FAANFAAN ChiefChief MedicalMedical--ScientificScientific OfficerOfficer DirectorDirector ofof ClinicalClinical ResearchResearch SunSun HealthHealth ResearchResearch InstituteInstitute FailingFailing MemoryMemory:: TheThe ProblemProblem •• ADAD isis thethe 77th leadingleading causecause ofof deathdeath inin thethe USUS •• ADAD affectsaffects 5.15.1 millionmillion AmericansAmericans •• ADAD isis thethe leadingleading causecause ofof longlong termterm carecare placementplacement andand accountsaccounts forfor upup toto 60%60% ofof LTCLTC InsuranceInsurance claimsclaims •• $100$100 billionbillion isis spentspent annuallyannually inin thethe USUS forfor ADAD relatedrelated costscosts andand expensesexpenses •• ByBy 2010,2010, ADAD willwill affectaffect oneone inin tenten overover ageage 6565 andand thethe costcost ofof carecare willwill raiseraise toto $160$160 billionbillion SummarySummary ofof PrevalencePrevalence andand ImpactImpact ofof ADAD onon SocietalSocietal CostsCosts ••>> 100,000100,000 peoplepeople diedie fromfrom ADAD perper yearyear ••ItIt isis estimatedestimated thatthat 1414 millionmillion AmericansAmericans willwill havehave ADAD byby thethe yearyear 20502050 ••AA costcost ofof $45,000$45,000 perper patientpatient perper yearyear ••AlzheimerAlzheimer’’ss patients/familiespatients/families spendspend >> $200,000$200,000 overover thethe remainderremainder ofof thethe patientpatient’’ss lifelife ••>50%>50% ofof nursingnursing homehome residentsresidents havehave AlzheimerAlzheimer’’ss diseasedisease 1. Ernst R et al. Cognitive Function and the Costs of Alzheimer’s Disease Arch Neurol. 1997;687-693. 2. Ernst RL, Hay JW. The US Economic and Social Costs of Alzheimer’s Disease Revisited. Am J Pub Health. 1994;84:1263 INCIDENCEINCIDENCE OFOF COMMONCOMMON NEUROLOGICALNEUROLOGICAL DISEASESDISEASES Incidence New Cases Disease (per 100,000) (per year) Dementia 268 670,000 Alzheimer’s disease 188 470,000 Stroke 200 500,000 Seizures 50 124,000 Parkinson’s disease 16 40,000 Primary neoplasm 15 37,500 Amyotrophic lateral sclerosis 6 15,000 Primary brain tumor 6 15,000 Multiple sclerosis 2 5,000 Gullain Barre’ 1 2,500 Huntington’s disease 0.3 750 DifferentialDifferential DiagnosisDiagnosis ofof DementiaDementia • Alzheimer’s Disease (AD) • Dementia with Lewy Bodies (DLB) • AD & Vascular Dementia (mixed) • Vascular Dementia • Frontotemporal Dementia (FTD) • Parkinson’s Disease • Huntington’s Disease • Other Degenerative Diseases (PSP, OPCA, ALS with dementia) • Dementias Secondary to Alcohol • Depression/Pseudodementia • Normal Pressure Hydrocephalus (NPH) • Structural Lesions • Metabolic Disorders (Hypothyroidism) • Infections (e.g. neurosyphillis, AIDS, CJD) • Drug Intoxication RiskRisk FactorsFactors forfor CognitiveCognitive DeclineDecline z age z genetic influences z ApoE status z female gender • medical comorbidities RiskRisk FactorsFactors forfor CognitiveCognitive Decline:Decline: MedicalMedical ComorbiditiesComorbidities •• HypertensionHypertension •• HeartHeart diseasedisease •• DiabetesDiabetes •• ElevatedElevated lowlow--densitydensity lipoproteinlipoprotein cholesterolcholesterol •• HighHigh homocysteinehomocysteine levelslevels •• TransitoryTransitory ischemicischemic attacksattacks (TIAs)(TIAs) •• HeadHead traumatrauma •• EnvironmentalEnvironmental exposureexposure toto toxinstoxins (particularly(particularly lead)lead) RiskRisk FactorsFactors forfor CognitiveCognitive Decline:Decline: Psychological/PsychosocialPsychological/Psychosocial FactorsFactors •• LowLow educationaleducational achievementachievement •• LackLack ofof physicalphysical activityactivity •• LackLack ofof socialsocial interaction/leisureinteraction/leisure activitiesactivities •• ExcessiveExcessive responseresponse toto stressstress (excessive(excessive cortisolcortisol levels)levels) RiskRisk FactorsFactors forfor CognitiveCognitive Decline:Decline: LifestyleLifestyle ChoicesChoices •• SmokingSmoking •• SubstanceSubstance abuse,abuse, includingincluding alcoholalcohol andand illicitillicit drugsdrugs AlzheimerAlzheimer’’ss andand thethe BrainBrain AmyloidAmyloid PrecursorPrecursor ProteinProtein (APP)(APP) •• AA singlesingle membranemembrane-- spanningspanning protein,protein, whichwhich hashas aa largelarge extracellularextracellular aminoamino terminalterminal domaindomain andand smallsmall intracellularintracellular cytoplasmiccytoplasmic domaindomain1 •• UndergoesUndergoes regulatedregulated intramembraneintramembrane proteolysisproteolysis viavia membranemembrane--boundbound 2 1. Turner PR, et al. Prog Neurobiol. 2003;70(1):1-32. proteasesproteases 2. Haass C, Selkoe DJ. Nat Rev Mol Cell Biol. 2007;8(2):101-112. αα,, γγ SecretaseSecretase Pathway:Pathway: NoNo AAββ FormationFormation sAPPα APP p3 α secretase γ secretase AICD •• Cleavage is catalyzed by α and γ secretases, respectively, producing sAPPα, p3 peptide, and an APP intracellular 20 domaindi(AICD) (AICD) ββ,, γγ SecretaseSecretase Pathway:Pathway: AAββ FormationFormation Amyloid sAPP β plaque APP Aβ Oligomers β secretase γ secretase AICD • Cleavage is catalyzed by β and γ secretases • The γ cleavage site is within the transmembrane 21 γγ SecretaseSecretase •• AnAn aspartylaspartyl proteaseprotease complexcomplex composedcomposed ofof APH1,APH1, nicastrinnicastrin,, PS1PS1 oror PS2,PS2, andand PEN2PEN2 •• CleavesCleaves APPAPP followingfollowing APPAPP scissionscission byby ββ secretasesecretase •• SiteSite ofof cleavagecleavage isis variablevariable andand cancan occuroccur afterafter AAββ38,, AAββ40,, oror AAββ42 –– SiteSite ofof cleavagecleavage determinesdetermines selfself--aggregatingaggregating potentialpotential andand pathogenicitypathogenicity ofof AAββ –– AAββ42 hashas strongstrong propensitypropensity toto oligomerizeoligomerize inin vivovivo Haass C, Selkoe DJ. Nat Rev Mol Cell Biol. 2007;8(2):101-112. AAββ OligomersOligomers andand AAββ Plaques:Plaques: TheoriesTheories onon NeurotoxicityNeurotoxicityAmyloid plaque •• WhichWhich AAββ formform isis toxictoxic toto thethe neuron?neuron? –– AAββ oligomersoligomers •• Induce synaptic 1 dysfunction? Aβ •• Decrease hippocampal Oligomers plasticity?1,2 –– AAββ plaquesplaques •• By-product of AD only?3 AICD •• Interferes with dendritic 4 signal transmission? 1. Turner PR, et al. Prog Neurobiol. 2003;70(1):1-32. 2. Puzzo D, et al. J Neurosci. 2005;25(29):6887-6897. 3. Hull M, et al. Drugs. 2006;66(16):2075-2093. 25 4. Spires TL, et al. J Neurosci. 2005;25(31):7278-7287. ββ--amyloidamyloid –– TThehe CoreCore ofof thethe SenileSenile PlaquesPlaques Lipid Amyloid Membrane INTRACELLULAR Precursor Protein (APP) Beta amyloid β-secretase γ-secretase EXTRACELLULAR α-secretase Senile Plaque Aβ 40 Aβ 42 Soluble forms β Pleated Sheet Relkin, 2006. Amyloid Angiopathy ββ--AmyloidAmyloid––relatedrelated APP gene Production diseasedisease--modifyingmodifying strategiesstrategies ? APP Cu++ Aβ ? Chelator Monomer Immunotherapy Antisense Aβ ? Oligomer Secretase modulators Aggregation Aβ Fibril Deposition Fibrillogenesis Diffuse modulators Plaque Senile Relkin, 2006. Anti- Plaque inflammatory γγ SecretaseSecretase InhibitionInhibition Plasma Aβ Liver clearance Blood-brain barrier Aβ Interstitial CSF space Aβ Amyloid plaque Brain APP Oligomers sAPP β γ secretase Intracellular AICD β secretase 28 CSF=cerebrospinal fluid. AmyloidAmyloid CascadeCascade HypothesisHypothesis Increased Aβ Production Decreased Aβ Clearance Increased Aβ Monomers, Oligomers, and Fibrils Aβ Plaque Deposition Synaptic Dysfunction Neuronal Death, Atrophy of the Cortex, Hippocampus, and Amygdala Adapted from: Lichtlen P, Mohajeri MH. J Neurochem. 2008;104(4):859-874. Parameshwaran K, et al. Exp Neurol. [Epub ahead of print]. Evin G, et al. CNS Drugs. 2006;20(5):351-372. •• Progressive, irreversible ADAD ProgressionProgression brain disorder which is not a part of normal not a part of normal Healthy aging Amnestic MCI Clinically diagnosed AD aging1 AD brain Amnestic MCI: • Insidious onset of changes may memory problems; Cognitive • start decades other cognitive decline before functions OK; brain accelerates early symptoms often symptoms compensates for after AD mistaken for age-related show changes diagnosis 1 memory change Normal age-related •• Disease progression memory loss leads to behavioral and 1 cognitive changes Total loss of independent •• Variable disease function progression and rate 1 of decline Birth 40 60 80 Death •• Risk factors: aging, Life Course 1 MCI=mild cognitive impairment. family history , head 1. US Department of Health and Human Services. 2005-2006 Progress Report on Alzheimer's Disease, 2007. injuryinjury2 2. Van Den Heuvel C, et al. Prog Brain Res. 2007;161:303-316. WhatWhat cancan youyou do?do? MaintainMaintain YourYour Brain:Brain: MakeMake brainbrain healthyhealthy lifelife choiceschoices •• BeBe heartheart smartsmart •• AdoptAdopt aa brainbrain healthyhealthy dietdiet •• StayStay physicallyphysically activeactive •• StayStay mentallymentally activeactive •• AlzheimerAlzheimer’’ss preventionprevention startsstarts now!now! BeBe HeartHeart SmartSmart •• OptimizeOptimize bloodblood pressurepressure control.control. (Certain(Certain typestypes ofof diuretics,diuretics, betabeta blockersblockers andand dihydropyridinedihydropyridine CaCa++ channelchannel blockers)blockers) •• DonDon’’tt smokesmoke •• ReduceReduce homocysteinehomocysteine levelslevels •• KeepKeep diabetesdiabetes underunder control.control. (SQ(SQ InsulinInsulin andand
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