0000000000512871

AUTHOR

Sandra Amor

showing 2 related works from this author

Control of spasticity in a multiple sclerosis model using central nervous system-excluded CB1 cannabinoid receptor agonists

2014

The purpose of this study was the generation of central nervous system (CNS)-excluded cannabinoid receptor agonists to test the hypothesis that inhibition of spasticity, due to CNS autoimmunity, could be controlled by affecting neurotransmission within the periphery. Procedures included identification of chemicals and modeling to predict the mode of exclusion; induction and control of spasticity in the ABH mouse model of multiple sclerosis; conditional deletion of CB1 receptor in peripheral nerves; side-effect profiling to demonstrate the mechanism of CNS-exclusion via drug pumps; genome-wide association study in N2(129×ABH) backcross to map polymorphic cannabinoid drug pump; and sequencing…

Central Nervous SystemCannabinoid receptorEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosismedicine.medical_treatmentCentral nervous systemPharmacologyBiologyBiochemistryMiceReceptor Cannabinoid CB1GeneticsmedicineAnimalsSpasticityMolecular BiologyCannabinoid Receptor AgonistsCannabinoidsMultiple sclerosisExperimental autoimmune encephalomyelitisCannabinoid Receptor Agonistsmedicine.disease3. Good healthmedicine.anatomical_structureAjulemic acidMuscle SpasticityFemaleCannabinoidmedicine.symptomMultidrug Resistance-Associated ProteinsBiotechnologymedicine.drug
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BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions

2011

Several lines of evidence indicate that remyelination represents one of the most effective mechanisms to achieve axonal protection. For reasons that are not yet understood, this process is often incomplete or fails in multiple sclerosis (MS). Activated astrocytes appear to be able to boost or inhibit endogenous repair processes. A better understanding of remyelination in MS and possible reasons for its failure is needed. Using the well-established toxic demyelination cuprizone model, we created lesions with either robust or impaired endogenous remyelination capacity. Lesions were analyzed for mRNA expression levels by Affymetrix GeneChip® arrays. One finding was the predominance of immune a…

MalePathologyPlatelet-derived growth factormedicine.medical_treatmentCell CountBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineFluorescent Antibody Technique IndirectOligonucleotide Array Sequence AnalysisPlatelet-Derived Growth Factor0303 health sciencesGlial fibrillary acidic proteinbiologyExperimental autoimmune encephalomyelitisAstrocytomaMiddle AgedImmunohistochemistrymedicine.anatomical_structureFemaleFibroblast Growth Factor 2Fatty Acid-Binding Protein 7Adultmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyBlotting WesternNerve Tissue ProteinsFatty Acid-Binding ProteinsReal-Time Polymerase Chain ReactionTransfection03 medical and health sciencesCuprizoneCell Line TumorGlial Fibrillary Acidic ProteinmedicineAnimalsHumansRNA MessengerRemyelination030304 developmental biologyAgedEndocrine and Autonomic SystemsMultiple sclerosisGrowth factorTumor Suppressor Proteinsmedicine.diseaseOligodendrocyteMice Inbred C57BLchemistryAstrocytesbiology.proteinOsteopontinCarrier Proteins030217 neurology & neurosurgeryDemyelinating Diseases
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