2024
Repetitive Mild Closed-Head Injury Induced Synapse Loss and Increased Local BOLD-fMRI Signal Homogeneity
Markicevic M, Mandino F, Toyonaga T, Cai Z, Fesharaki-Zadeh A, Shen X, Strittmatter S, Lake E. Repetitive Mild Closed-Head Injury Induced Synapse Loss and Increased Local BOLD-fMRI Signal Homogeneity. Journal Of Neurotrauma 2024 PMID: 39096127, DOI: 10.1089/neu.2024.0095.Peer-Reviewed Original ResearchChronic variable stressRegional homogeneityFunctional brain abnormalitiesSynapse densityMild closed-head injuryClosed-head injuryTraumatic brain injuryTreat traumatic brain injuryNeurobiological alterationsMild head injuryVariable stressBrain abnormalitiesPositron emission tomographyMultimodal studiesSynaptic densityMagnetic resonance imagingBrain imagingBrain injuryInduce synapse lossFMRIInjured miceMouse modelEmission tomographyResonance imagingCompensatory mechanismsAn overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms
Fesharaki-Zadeh A, Datta D. An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms. Frontiers In Cellular Neuroscience 2024, 18: 1371213. PMID: 38682091, PMCID: PMC11045909, DOI: 10.3389/fncel.2024.1371213.Peer-Reviewed Original ResearchClosed-Head Impact Model of Engineered Rotational AccelerationModel of traumatic brain injuryPreclinical modelsPreclinical models of traumatic brain injuryAnimal modelsTraumatic brain injuryControlled cortical impact injuryRodent preclinical modelsDisease modifying effectFluid percussion injuryCortical impact injuryBlast injuryAnimal models of traumatic brain injuryBrain injuryMotor vehicle accidentsTherapeutic regimenPathophysiological mechanismsEtiology of traumatic brain injuryPharmacological agentsSports related injuriesInjury modelCalcium dysregulationPrevalence of traumatic brain injuryClinical treatmentClinical settingCombined Use of Guanfacine and N-Acetylcysteine for the Treatment of Cognitive Deficits After Traumatic Brain Injury
Khasnavis S, Belliveau T, Arnsten A, Fesharaki-Zadeh A. Combined Use of Guanfacine and N-Acetylcysteine for the Treatment of Cognitive Deficits After Traumatic Brain Injury. Neurotrauma Reports 2024, 5: 226-231. PMID: 38524728, PMCID: PMC10960163, DOI: 10.1089/neur.2023.0124.Peer-Reviewed Original ResearchTreatment of cognitive deficitsTraumatic brain injuryExecutive functionCognitive deficitsTraumatic brain injury clinicEfficacy of guanfacinePre-frontal cortexBrain injuryTreat traumatic brain injuryBehavioral therapyNeuropsychological testsCognitive symptomsCognitive changesPlacebo-controlled trialProcessing speedGuanfacineCortical functionOpen-label useApproved medicationsPersonsPost-treatmentDeficitsTraumatizationN-acetylcysteineMTBI
2023
Navigating the Complexities of Traumatic Encephalopathy Syndrome (TES): Current State and Future Challenges
Fesharaki-Zadeh A. Navigating the Complexities of Traumatic Encephalopathy Syndrome (TES): Current State and Future Challenges. Biomedicines 2023, 11: 3158. PMID: 38137378, PMCID: PMC10740836, DOI: 10.3390/biomedicines11123158.Peer-Reviewed Original ResearchTraumatic encephalopathy syndromeChronic traumatic encephalopathyTraumatic brain injuryRepetitive head impactsEncephalopathy syndromeHeterogeneity of TBIUnique neurodegenerative diseaseEffective clinical treatmentClinical research studiesEarly diagnostic methodsClinical featuresClinical manifestationsTraumatic encephalopathyRange of treatmentsBrain injuryNeuroimaging markerClinical identificationNeurodegenerative conditionsAlzheimer's diseaseClinical treatmentClinical settingClinical researchNeurodegenerative diseasesNeuropathological phenomenaDisease
2022
Oxidative Stress in Traumatic Brain Injury
Fesharaki-Zadeh A. Oxidative Stress in Traumatic Brain Injury. International Journal Of Molecular Sciences 2022, 23: 13000. PMID: 36361792, PMCID: PMC9657447, DOI: 10.3390/ijms232113000.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryAntioxidant therapyBrain injuryClinical settingPost-traumatic brain injuryOxidative stressReactive oxygen speciesUnderlying pathophysiological mechanismsSecondary injury cascadePromising treatment optionLipid peroxidation productsFree radical generating enzymesReal clinical settingNeurometabolic cascadeFree radical scavengerInjury cascadeChronic inflammationPathophysiological mechanismsSynaptic dysfunctionPost injuryTreatment optionsTBI treatmentSide effectsTBI symptomsInjury
2021
A Case of Possible Chronic Traumatic Encephalopathy and Alzheimer’s Disease in an Ex-Football Player
Fesharaki-Zadeh A. A Case of Possible Chronic Traumatic Encephalopathy and Alzheimer’s Disease in an Ex-Football Player. The Neurologist 2021, 27: 249-252. PMID: 34879014, PMCID: PMC9439689, DOI: 10.1097/nrl.0000000000000391.Peer-Reviewed Original ResearchConceptsChronic traumatic encephalopathyTraumatic encephalopathyAlzheimer's diseasePrior traumatic brain injuryBehavioral variant frontotemporal dementiaRepetitive head traumaTraumatic brain injuryPrior psychiatric historyPrimary progressive aphasiaVariant frontotemporal dementiaPositron emission tomographyCTE casesClinical presentationHead traumaCase reportClinical historyDefinitive diagnosisClinical algorithmBrain injuryComorbid moodPsychiatric historyCerebrospinal fluidNeuroimaging biomarkersProgressive aphasiaFrontotemporal dementia
2020
Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in
Chiasseu M, Fesharaki-Zadeh A, Saito T, Saido TC, Strittmatter SM. Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-in. Neurobiology Of Disease 2020, 145: 105059. PMID: 32858147, PMCID: PMC7572902, DOI: 10.1016/j.nbd.2020.105059.Peer-Reviewed Original ResearchConceptsMild traumatic brain injuryTraumatic brain injuryAlzheimer's diseaseBrain injuryGene-environment interactionsMild closed head injuryMorris water maze testAge-matched wild-type controlsStrong unmet needAccumulation of amyloidAge-matched miceClosed head injuryWater maze testNovel object recognitionPersistent cognitive deficitsProtein gene mutationsIba1 expressionWild-type controlsPhospho-tauClinical manifestationsAD pathologyAD symptomsHead injuryAD pathogenesisRisk factorsIncreased Behavioral Deficits and Inflammation in a Mouse Model of Co-Morbid Traumatic Brain Injury and Post-Traumatic Stress Disorder
Fesharaki-Zadeh A, Miyauchi JT, St. Laurent-Arriot K, Tsirka SE, Bergold PJ. Increased Behavioral Deficits and Inflammation in a Mouse Model of Co-Morbid Traumatic Brain Injury and Post-Traumatic Stress Disorder. ASN Neuro 2020, 12: 1759091420979567. PMID: 33342261, PMCID: PMC7755938, DOI: 10.1177/1759091420979567.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryPost-traumatic stress disorderChi groupBrain injuryBarnes mazeCo-morbid traumatic brain injuryMale C57/BL6 miceCognitive deficitsComorbid post-traumatic stress disorderC57/BL6 miceStress disorderClosed-head modelIba-1 levelsChronic variable stress modelActive place avoidancePlace avoidanceGreater cognitive deficitsNeuroinflammatory outcomesBasal anxiety levelsCVS groupSham treatmentBL6 miceBehavioral deficitsMouse modelKey underlying mechanism
2019
Chronic Traumatic Encephalopathy: A Brief Overview
Fesharaki-Zadeh A. Chronic Traumatic Encephalopathy: A Brief Overview. Frontiers In Neurology 2019, 10: 713. PMID: 31333567, PMCID: PMC6616127, DOI: 10.3389/fneur.2019.00713.Peer-Reviewed Original ResearchChronic traumatic encephalopathyTraumatic brain injuryRepetitive mild traumatic brain injuryPost-traumatic brain injuryMild traumatic brain injuryPeri-vascular regionsRisk factor genesAmerican football playersTraumatic encephalopathyAPOE4 carriersSubtle presentationBrain injuryTBI treatmentTeam physiciansNeuropathological signatureNeuropsychiatric assessmentPhosphorylated tauCognitive impairmentCombat settingNeurodegenerative diseasesDiseaseMilitary veteransDistinct phenotypesSubtypesFootball players