2021
Therapy for Alzheimer’s disease: Missing targets and functional markers?
Stoiljkovic M, Horvath TL, Hajós M. Therapy for Alzheimer’s disease: Missing targets and functional markers? Ageing Research Reviews 2021, 68: 101318. PMID: 33711510, PMCID: PMC8131215, DOI: 10.1016/j.arr.2021.101318.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseNew symptomatic treatmentsNeural network integrityClinical characteristicsNext-generation therapiesSymptomatic treatmentOutcome biomarkerTau pathologyFluid biomarkersPlasma biomarkersDisease progressionEffective therapyNeurophysiological biomarkersTreatment candidatesCerebrospinal fluidNovel biomarkersTranslational studiesTreatment interventionsDiseaseTarget engagementTherapyBiomarkersCurrent conceptsMultiple biomarkersDrug targets
2017
4.19 Obesity and Appetite: Central Control Mechanisms
Horvath T. 4.19 Obesity and Appetite: Central Control Mechanisms. 2017, 369-376. DOI: 10.1016/b978-0-12-803592-4.00085-7.Peer-Reviewed Original ResearchLate-onset chronic diseasesChronic diseasesPrevalence of obesitySerious comorbiditiesFat massTissue malignancyParkinson's diseaseCardiovascular disordersCentral control mechanismAlzheimer's diseaseDiseaseEpigenetic vulnerabilityCellular energy metabolismObesityVulnerable individualsEnergy metabolismAppetiteDisordersTissueDifferent tissuesComorbiditiesDiabetesMajor roleMalignancySatiety
2015
Synaptic lipids in cortical function and psychiatric disorders
Stutz B, Horvath TL. Synaptic lipids in cortical function and psychiatric disorders. EMBO Molecular Medicine 2015, 8: 3-5. PMID: 26671988, PMCID: PMC4718156, DOI: 10.15252/emmm.201505749.Peer-Reviewed Original ResearchConceptsPsychiatric disordersClinical therapeutic strategiesPathophysiologic mechanismsCortical circuitryCortical functionExcitatory neuronsTherapeutic strategiesAnimal modelsReliable biomarkersPsychiatric diseasesPsychiatric consequencesEMBO Molecular MedicinePsychiatric conditionsMillions of peopleHuman subjectsCircuit functionDisordersLipidsMolecular medicinePatientsPathophysiologyEtiologyDiseaseMiceNeuronsHypothalamic Agrp Neurons Drive Stereotypic Behaviors beyond Feeding
Dietrich MO, Zimmer MR, Bober J, Horvath TL. Hypothalamic Agrp Neurons Drive Stereotypic Behaviors beyond Feeding. Cell 2015, 160: 1222-1232. PMID: 25748653, PMCID: PMC4484787, DOI: 10.1016/j.cell.2015.02.024.Peer-Reviewed Original ResearchConceptsHypothalamic AgRP neuronsAgRP neuronsNeuropeptidergic signalingReceptor signalingFunctional rolePotential therapeutic avenuesAgRP neuron activationStereotypic behaviorFeeding behaviorRepetitive behaviorsSignalingTherapeutic avenuesFood triggersAdult miceNervous systemDecreased anxietyNeuronsMinor effectActivationFood consumptionNeuron activationGoal-directed behaviorSensory informationFlexible goal-directed behaviorDiseaseThe ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease
Youm YH, Nguyen KY, Grant RW, Goldberg EL, Bodogai M, Kim D, D'Agostino D, Planavsky N, Lupfer C, Kanneganti TD, Kang S, Horvath TL, Fahmy TM, Crawford PA, Biragyn A, Alnemri E, Dixit VD. The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease. Nature Medicine 2015, 21: 263-269. PMID: 25686106, PMCID: PMC4352123, DOI: 10.1038/nm.3804.Peer-Reviewed Original Research
2012
A marriage made to last in drug design
Dietrich MO, Horvath TL. A marriage made to last in drug design. Nature Medicine 2012, 18: 1737-1738. PMID: 23223057, DOI: 10.1038/nm.3018.Peer-Reviewed Original ResearchGhrelin Regulation of Learning, Memory, and Neurodegeneration
Horvath T. Ghrelin Regulation of Learning, Memory, and Neurodegeneration. Contemporary Endocrinology 2012, 171-180. DOI: 10.1007/978-1-61779-903-7_9.Peer-Reviewed Original ResearchLate-onset chronic diseasesChronic diseasesGut-derived hormonesCause of morbidityChronic disease developmentGhrelin regulationGhrelin actionPeripheral mechanismsBrain healthTissue malignancyCardiovascular disordersParkinson's diseaseCalorie restrictionBrain functionDiseaseProlongs longevityEpigenetic vulnerabilityFinancial burdenGhrelinCellular energy metabolismDisease developmentEnergy metabolismIntegrative physiologyTissueHealth
2011
Mitochondrial uncoupling protein 2 (UCP2) in glucose and lipid metabolism
Diano S, Horvath TL. Mitochondrial uncoupling protein 2 (UCP2) in glucose and lipid metabolism. Trends In Molecular Medicine 2011, 18: 52-58. PMID: 21917523, DOI: 10.1016/j.molmed.2011.08.003.Peer-Reviewed Original ResearchConceptsProtein 2Lipid metabolismExcess of nutrientsHypothalamic neuronal circuitsNutrient availabilityPeripheral tissue functionsPhysiological functionsMetabolism regulationChronic diseasesMetabolism-related chronic diseasesTissue functionFuture therapeutic strategiesPathological processesPeripheral mechanismsLipid levelsNeuronal circuitsTherapeutic strategiesMetabolismImpairs healthMitochondriaDiseaseUCP2GlucoseRegulationNutrients
2006
Uncoupling protein‐2 promotes nigrostriatal dopamine neuronal function
Andrews ZB, Rivera A, Elsworth JD, Roth RH, Agnati L, Gago B, Abizaid A, Schwartz M, Fuxe K, Horvath TL. Uncoupling protein‐2 promotes nigrostriatal dopamine neuronal function. European Journal Of Neuroscience 2006, 24: 32-36. PMID: 16882005, DOI: 10.1111/j.1460-9568.2006.04906.x.Peer-Reviewed Original ResearchMeSH Keywords3,4-Dihydroxyphenylacetic AcidAnimalsCorpus StriatumDopamineDopamine Plasma Membrane Transport ProteinsImmunohistochemistryIon ChannelsMaleMembrane Transport ProteinsMiceMice, KnockoutMitochondrial ProteinsMotor ActivityNeuronsSubstantia NigraTyrosine 3-MonooxygenaseUncoupling Protein 2ConceptsSubstantia nigra pars compactaDopamine neuronal functionUCP2-KO miceParkinson's diseaseNeuronal functionNigrostriatal dopamine functionTyrosine hydroxylase immunoreactivityUCP2 knockout miceDopamine transporter immunoreactivityProtein 2Wild-type controlsHydroxylase immunoreactivityPars compactaDopamine turnoverTransporter immunoreactivityDopamine ratioBehavioral deficitsLocomotor functionNucleus accumbensBiochemical deficitsDopamine functionBrain regionsNeurological pathologiesDiseaseMice
2005
Uncoupling protein 2 protects dopaminergic neurons from acute 1,2,3,6‐methyl‐phenyl‐tetrahydropyridine toxicity
Conti B, Sugama S, Lucero J, Winsky‐Sommerer R, Wirz SA, Maher P, Andrews Z, Barr AM, Morale MC, Paneda C, Pemberton J, Gaidarova S, Behrens MM, Beal F, Sanna PP, Horvath T, Bartfai T. Uncoupling protein 2 protects dopaminergic neurons from acute 1,2,3,6‐methyl‐phenyl‐tetrahydropyridine toxicity. Journal Of Neurochemistry 2005, 93: 493-501. PMID: 15816872, DOI: 10.1111/j.1471-4159.2005.03052.x.Peer-Reviewed Original ResearchConceptsDopaminergic neuronsParkinson's diseaseOxidative stressSpecific neuronal expressionTyrosine hydroxylase promoterTetrahydropyridine (MPTP) toxicityCatecholaminergic neuronsSubstantia nigraHydroxylase promoterLocomotor functionMouse modelNeuronal expressionAcute exposureTransgenic miceSporadic formsTwofold elevationUCP2 expressionDiseaseMarked reductionNeuronsMiceNeuroprotectionProtein 2UCP familyDrug targets
2003
Coenzyme Q Induces Nigral Mitochondrial Uncoupling and Prevents Dopamine Cell Loss in a Primate Model of Parkinson’s Disease
Horvath TL, Diano S, Leranth C, Garcia-Segura LM, Cowley MA, Shanabrough M, Elsworth JD, Sotonyi P, Roth RH, Dietrich EH, Matthews RT, Barnstable CJ, Redmond DE. Coenzyme Q Induces Nigral Mitochondrial Uncoupling and Prevents Dopamine Cell Loss in a Primate Model of Parkinson’s Disease. Endocrinology 2003, 144: 2757-2760. PMID: 12810526, DOI: 10.1210/en.2003-0163.Peer-Reviewed Original ResearchConceptsDopamine cell lossParkinson's diseaseCell lossShort-term oral administrationMitochondrial uncouplingSubstantia nigraDopamine neuronsTetrahydropyridine (MPTP) administrationCoenzyme QPrimate modelOral administrationDiseaseOxidative stressState 4 respirationMitochondrial uncoupling proteinAdministrationUncoupling proteinUncouplingNeuronsNigraTetrahydropyridine
2000
Estrogen Is Essential for Maintaining Nigrostriatal Dopamine Neurons in Primates: Implications for Parkinson's Disease and Memory
Leranth C, Roth R, Elsworth J, Naftolin F, Horvath T, Redmond D. Estrogen Is Essential for Maintaining Nigrostriatal Dopamine Neurons in Primates: Implications for Parkinson's Disease and Memory. Journal Of Neuroscience 2000, 20: 8604-8609. PMID: 11102464, PMCID: PMC6773080, DOI: 10.1523/jneurosci.20-23-08604.2000.Peer-Reviewed Original ResearchConceptsNigrostriatal dopamine neuronsDopamine neuronsParkinson's diseaseSubstantia nigraDopamine cellsTyrosine hydroxylase-expressing neuronsTyrosine hydroxylase-immunoreactive cellsNigral dopamine systemsEstrogen replacement therapyNew treatment strategiesUnbiased stereological analysisTypes of neuronsProgression of diseaseEstrogen replacementPostmenopausal womenEstrogen deprivationReplacement therapyTreatment strategiesCompact zoneGonadal hormonesLong-term effectsDopamine systemEstrogenDiseaseNeurons