Matthew Alsaloum, PhD
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About
Education & Training
- PhD
- Yale School of Medicine, Interdepartmental Neuroscience Program (2021)
- BS
- Stony Brook University, Biology (Neuroscience) (2015)
Research
Overview
Medical Subject Headings (MeSH)
Pain
ORCID
0000-0002-9832-0138
Research at a Glance
Yale Co-Authors
Frequent collaborators of Matthew Alsaloum's published research.
Publications Timeline
A big-picture view of Matthew Alsaloum's research output by year.
Research Interests
Research topics Matthew Alsaloum is interested in exploring.
Shujun Liu
Grant Higerd-Rusli, PhD
Peng Zhao, PhD
Stephen Waxman, MD, PhD
Sidharth Tyagi, MS
Sulayman Dib-Hajj, PhD
12Publications
315Citations
Publications
2022
Depolarizing NaV and Hyperpolarizing KV Channels Are Co-Trafficked in Sensory Neurons
Higerd-Rusli GP, Alsaloum M, Tyagi S, Sarveswaran N, Estacion M, Akin EJ, Dib-Hajj FB, Liu S, Sosniak D, Zhao P, Dib-Hajj SD, Waxman SG. Depolarizing NaV and Hyperpolarizing KV Channels Are Co-Trafficked in Sensory Neurons. Journal Of Neuroscience 2022, 42: 4794-4811. PMID: 35589395, PMCID: PMC9188389, DOI: 10.1523/jneurosci.0058-22.2022.Peer-Reviewed Original ResearchCitationsAltmetricConceptsIon channel traffickingMembrane proteinsChannel traffickingAxonal membrane proteinsTransport vesiclesPhysiological functionsSame vesiclesAxonal proteinsSpecific transport vesiclesIon channelsTrafficking of NaDiverse physiological functionsExcitability disordersDifferent physiological functionsDistinct ion channelsSensory neuron membraneSensory neuronsDistinct functional classesDistinct functional rolesNormal neuronal excitabilityTrafficking mechanismsNeuronal excitabilityPlasma membraneTherapeutic strategiesPrecise regulationStem cell-derived sensory neurons modelling inherited erythromelalgia: normalization of excitability
Alsaloum M, Labau JIR, Liu S, Effraim P, Waxman SG. Stem cell-derived sensory neurons modelling inherited erythromelalgia: normalization of excitability. Brain 2022, 146: 359-371. PMID: 35088838, PMCID: PMC10060693, DOI: 10.1093/brain/awac031.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSensory neuronsPluripotent stem cell-derived sensory neuronsDynamic clamp electrophysiologyMediators of painUnmet healthcare needsEffective therapeutic approachErythromelalgia mutationAmeliorate painNeuronal hyperexcitabilityPain disordersClinical studiesNeuronal excitabilityPreclinical studiesTherapeutic approachesEffective treatmentNaV1.7 currentsBaseline levelsClamp electrophysiologyHealthcare needsNav1.7 channelsPainErythromelalgiaHyperexcitabilityFunction mutationsNav1.7Evaluation of the Content of Ophthalmology Fellowship Program Web sites
Alsaloum P, Alsaloum M, Kim T, Zheng D, Valentim C, Muste J, Goshe J, Singh R. Evaluation of the Content of Ophthalmology Fellowship Program Web sites. Journal Of Academic Ophthalmology 2022, 14: e127-e132. PMID: 37388469, PMCID: PMC9928003, DOI: 10.1055/s-0042-1747673.Peer-Reviewed Original ResearchAltmetricConceptsMAIN OUTCOMEOphthalmology subspecialtiesCross-sectional studyFellowship programsHospital affiliationWellness programsSignificant heterogeneitySubspecialtySurgical statisticsSignificant differencesCurrent fellowsOutcomesProgram demographicsDemographic criteriaProgram Web sitesCase diversityCriteriaAverage numberProgram description
2021
Lacosamide Inhibition of NaV1.7 Channels Depends on its Interaction With the Voltage Sensor Domain and the Channel Pore
Labau JIR, Alsaloum M, Estacion M, Tanaka B, Dib-Hajj FB, Lauria G, Smeets HJM, Faber CG, Dib-Hajj S, Waxman SG. Lacosamide Inhibition of NaV1.7 Channels Depends on its Interaction With the Voltage Sensor Domain and the Channel Pore. Frontiers In Pharmacology 2021, 12: 791740. PMID: 34992539, PMCID: PMC8724789, DOI: 10.3389/fphar.2021.791740.Peer-Reviewed Original ResearchCitationsAltmetricContributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons
Alsaloum M, Labau JIR, Liu S, Estacion M, Zhao P, Dib-Hajj F, Waxman SG. Contributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons. Scientific Reports 2021, 11: 24283. PMID: 34930944, PMCID: PMC8688473, DOI: 10.1038/s41598-021-03608-x.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAction PotentialsAutopsyCell DifferentiationElectrophysiologyHumansImmunohistochemistryInduced Pluripotent Stem CellsMembrane PotentialsMutationNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelNeuronsNeurosciencesPainPatch-Clamp TechniquesProtein IsoformsSensory Receptor CellsSomatosensory CortexConceptsNeuronal excitabilitySomatosensory neuronsPluripotent stem cell-derived sensory neuronsDynamic clamp electrophysiologyTreatment of painPromising novel modalityVoltage-gated sodium channelsSodium channel isoformsNeuronal membrane potentialGenetic knockout modelsNav1.9 currentsPharmacologic blockSensory neuronsNav1.8Cellular correlatesRepetitive firingClamp electrophysiologyExcitabilityNeuronal backgroundNovel modalityChannel isoformsSodium channelsNeuronsNav1.9Knockout modelsiPSCs and DRGs: stepping stones to new pain therapies
Alsaloum M, Waxman SG. iPSCs and DRGs: stepping stones to new pain therapies. Trends In Molecular Medicine 2021, 28: 110-122. PMID: 34933815, PMCID: PMC8810720, DOI: 10.1016/j.molmed.2021.11.005.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsHuman DRG neuronsDRG neuronsDorsal root ganglion neuronsTreatment of painNovel pain therapeuticsNew pain therapiesVoltage-gated sodium channelsPain therapyPain therapeuticsGanglion neuronsTreatment optionsPain signalsSpinal cordPreclinical resultsPreclinical platformSensory neuronsPainNeuronsSodium channelsClinical translationIPSCsBlockadeCordTherapyExcitabilityA novel gain-of-function sodium channel β2 subunit mutation in idiopathic small fiber neuropathy
Alsaloum M, Labau JIR, Sosniak D, Zhao P, Almomani R, Gerrits M, Hoeijmakers JGJ, Lauria G, Faber CG, Waxman SG, Dib-Hajj S. A novel gain-of-function sodium channel β2 subunit mutation in idiopathic small fiber neuropathy. Journal Of Neurophysiology 2021, 126: 827-839. PMID: 34320850, PMCID: PMC8461825, DOI: 10.1152/jn.00184.2021.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSmall fiber neuropathyVoltage-gated sodium channel α-subunitsDorsal root ganglion neuronsSodium channel β subunitsSodium channel α subunitDiscernible causeChannel α-subunitsGanglion neuronsChannel β subunitΒ2 subunitIdiopathic small fiber neuropathySodium currentTetrodotoxin-resistant sodium currentTetrodotoxin-sensitive sodium currentPainful diabetic neuropathySubset of patientsUnmyelinated C-fibersCurrent-clamp analysisAction potential firingHuman pain disordersFirst evidenceNeuropathic painDiabetic neuropathyNeuronal hyperexcitabilityPain disordersPaclitaxel increases axonal localization and vesicular trafficking of Nav1.7
Akin EJ, Alsaloum M, Higerd GP, Liu S, Zhao P, Dib-Hajj FB, Waxman SG, Dib-Hajj SD. Paclitaxel increases axonal localization and vesicular trafficking of Nav1.7. Brain 2021, 144: 1727-1737. PMID: 33734317, PMCID: PMC8320304, DOI: 10.1093/brain/awab113.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDorsal root ganglion neuronsChemotherapy-induced peripheral neuropathyGanglion neuronsSensory axonsNav1.7 channelsPTX treatmentSensory neuronsHuman sensory neuronsEffect of paclitaxelSodium channel Nav1.7Chemotherapy drug paclitaxelAxonal vesicular transportConcentrations of paclitaxelNav1.7 mRNAInflammatory mediatorsNav1.7 expressionPeripheral neuropathyInflammatory milieuPrimary afferentsInflammatory conditionsChannel expressionChannel Nav1.7Nav1.7Increased expressionAxonal localization
2020
Status of peripheral sodium channel blockers for non-addictive pain treatment
Alsaloum M, Higerd GP, Effraim PR, Waxman SG. Status of peripheral sodium channel blockers for non-addictive pain treatment. Nature Reviews Neurology 2020, 16: 689-705. PMID: 33110213, DOI: 10.1038/s41582-020-00415-2.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and ConceptsConceptsPain conditionsPain treatmentDose-limiting adverse effectUnmet health care needsAdverse effectsMediators of painMultiple pain conditionsCommon pain conditionsCardiac adverse effectsTrigeminal ganglion neuronsTreatment of painDorsal root gangliaPeripheral nervous systemHuman pain disordersSodium channel blockersHealth care needsVoltage-gated sodium channelsImproved therapeutic agentsCurrent medicationsPain disordersPain managementGanglion neuronsRoot gangliaSafe treatmentClinical trials
2019
A gain-of-function sodium channel β2-subunit mutation in painful diabetic neuropathy
Alsaloum M, Estacion M, Almomani R, Gerrits MM, Bönhof GJ, Ziegler D, Malik R, Ferdousi M, Lauria G, Merkies IS, Faber CG, Dib-Hajj S, Waxman S. A gain-of-function sodium channel β2-subunit mutation in painful diabetic neuropathy. Molecular Pain 2019, 15: 1744806919849802. PMID: 31041876, PMCID: PMC6510061, DOI: 10.1177/1744806919849802.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDiabetic peripheral neuropathyPeripheral neuropathyNeuropathic painDiabetic peripheral neuropathy patientsPainful diabetic peripheral neuropathyDorsal root ganglion neuronsPainful diabetic neuropathyPeripheral neuropathy patientsSodium channel β subunitsSpectrum of patientsUse-dependent inhibitionCardiac conducting systemSodium channel α subunitVoltage-gated sodium channelsChannel α-subunitsSCN11A geneDiabetic neuropathyDiabetes mellitusChronic painNeuropathy patientsGanglion neuronsNegative genetic screeningChannel β subunitHealth sequelaeRepetitive stimulation