Search results for "Motoneurons"

showing 5 items of 5 documents

The serum level of free testosterone is reduced in amyotrophic lateral sclerosis

2002

Sporadic amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder affecting upper and lower motoneurons. There is an approximately 2:1 higher incidence of ALS in men compared to women, and this has raised the hypothesis of an involvement of sex hormones in the etiopathogenesis of the disorder. In this work, the serum levels of dehydroepiandrosterone sulphate (DHEAS), 17-betaestradiol, free and total testosterone were measured in 35 patients with defined or probable ALS, according to the El-Escorial/WFN revisited criteria, and compared to those obtained from 57 disease controls, matched for age and gender to the ALS group. We found no differences between ALS cases and …

Malemedicine.medical_specialtyCentral nervous system diseaseDehydroepiandrosterone sulphateDegenerative diseaseSex hormone-binding globulinInternal medicinemedicineHumans17-βestradiol; Amyotrophic lateral sclerosis; Dehydroepiandrosterone sulphate; Motoneurons; Sex hormone binding globulin; TestosteroneTestosteroneAmyotrophic lateral sclerosisAged17-βestradiolAged 80 and overSex Characteristicsbiologybusiness.industryTestosterone (patch)Middle Agedmedicine.diseaseAmyotrophic lateral sclerosisPathophysiologySex hormone binding globulinMotoneuronsEndocrinologyNeurologybiology.proteinFemaleNeurology (clinical)businessSex characteristicsHormone
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The Drosophila Hox gene Ultrabithorax acts both in muscles and motoneurons to orchestrate formation of specific neuromuscular connections

2016

Hox genes are known to specify motoneuron pools in the developing vertebrate spinal cord and to control motoneuronal targeting in several species. However, the mechanisms controlling axial diversification of muscle innervation patterns are still largely unknown. We present data showing that the Drosophila Hox gene Ultrabithorax (Ubx) acts in the late embryo to establish target specificity of ventrally projecting RP motoneurons. In abdominal segments A2 to A7, RP motoneurons innervate the ventrolateral muscles VL1-4, with VL1 and VL2 being innervated in a Wnt4-dependent manner. In Ubx mutants, these motoneurons fail to make correct contacts with muscle VL1, a phenotype partially resembling t…

0301 basic medicineCell typeEmbryo Nonmammaliananimal structuresNeuromuscular JunctionGenes InsectMuscle DevelopmentNeuromuscular junctionAnimals Genetically ModifiedHox genes03 medical and health sciencesWNT4MorphogenesismedicineAnimalsDrosophila ProteinsHox geneWnt Signaling PathwayMolecular BiologyTranscription factorUltrabithoraxHomeodomain ProteinsMotor NeuronsGeneticsbiologyMusclesmusculoskeletal neural and ocular physiologyfungiGenes HomeoboxGene Expression Regulation Developmentalbiology.organism_classificationMuscle innervationSegmental patterningCell biologyMotoneuronsDrosophila melanogaster030104 developmental biologymedicine.anatomical_structurenervous system209embryonic structuresDrosophilaWnt signalling pathwayDrosophila melanogasterDrosophila ProteinTranscription FactorsResearch ArticleDevelopmental BiologyDevelopment
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Grp78 overexpression triggers pink1-ip3 r-mediated neuroprotective mitophagy

2021

An experimental model of spinal root avulsion (RA) is useful to study causal molecular programs that drive retrograde neurodegeneration after neuron-target disconnection. This neurode-generative process shares common characteristics with neuronal disease-related processes such as the presence of endoplasmic reticulum (ER) stress and autophagy flux blockage. We previously found that the overexpression of GRP78 promoted motoneuronal neuroprotection after RA. After that, we aimed to unravel the underlying mechanism by carrying out a comparative unbiased proteomic analysis and pharmacological and genetic interventions. Unexpectedly, mitochondrial factors turned out to be most altered when GRP78…

biologyQH301-705.5Endoplasmic reticulumAutophagyNeurodegenerationMitophagyMedicine (miscellaneous)PINK1Mitochondrionmedicine.diseaseNeuroprotectionGeneral Biochemistry Genetics and Molecular BiologyArticleNeuroprotectionCell biologyGRP78/BiPMotoneuronsChaperone (protein)Mitophagybiology.proteinmedicineBiology (General)Neurodegeneration
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The Etiology of Muscle Fatigue Differs between Two Electrical Stimulation Protocols

2016

International audience; Purpose: This study aimed at investigating the mechanisms involved in the force reduction induced by two electrical stimulation (ES) protocols that were designed to activate motor units differently. Methods: The triceps surae of 11 healthy subjects (8 men; age, similar to 28 yr) was activated using ES applied over the tibial nerve. Two ES protocols (conventional [CONV]: 20 Hz, 0.05 ms vs wide-pulse high-frequency [WPHF]: 80 Hz, 1 ms) were performed and involved 40 trains (6 s on-6 s off) delivered at an intensity (I-ES) evoking 20% of maximal voluntary contraction. To analyze the mechanical properties of the motor units activated at I-ES, force-frequency relation was…

MaleStimulationElectromyographytorque decreaseplateau-like behaviorh-reflexchemistry.chemical_compound0302 clinical medicinemotor unit recruitmentOrthopedics and Sports Medicinehuman motoneuronsquadriceps femorismedicine.diagnostic_testChemistryPulse (signal processing)Anatomystimulation parametersHealthy VolunteersMuscle Fatiguetriceps surae[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Femalemedicine.symptomMuscle ContractionMuscle contractionAdultRecruitment Neurophysiologicalmedicine.medical_specialtyhuman skeletal-musclePhysical Therapy Sports Therapy and RehabilitationnervePhosphocreatineYoung Adult03 medical and health sciencesInternal medicineexcitabilitymedicineHumansMuscle SkeletalMuscle fatigueElectromyography030229 sport sciencesmagnetic resonance spectroscopyElectric StimulationEndocrinologyevoked contractions[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Motor unit recruitmentTibial NerveH-reflex030217 neurology & neurosurgeryMedicine & Science in Sports & Exercise
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Architecture of cell differentiation, stress-mediated protein expression and transport in iPSC-derived Motor Neurons bearing a pG376D TDP-43 mutation

2020

BACKGROUND AND RATIONALE. ALS is a fatal neurodegenerative disease caused by loss of motoneurons (MNs). Growingevidence suggests that the disease has a strong genetic basis. Up to now, more than 50 ALS-related genes have beenfound. Among these, TARDBP plays a critical role in ALS. Pathogenic mutations in TARDBP gene are found in 1–3% offamilial ALS cases. A few years ago, a novel G376D TARDBP mutation associated to ALS was reported (Conforti et al, 2011). Recently, a verylarge genealogic tree from this G376D family was made (2HE Association, personal communication) leading to a largecollection of DNA, plasma and fibroblasts (FBs) from several family members, both affected and not clinically…

Motoneurons iPSC Transcriptomics
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