Search results for "Neuromuscular"

showing 10 items of 363 documents

Evidence of resistance training-induced neural adaptation in older adults

2021

The deleterious effects of aging on force production are observable from the age of 40 upwards, depending on the measure. Neural mechanisms contributing to maximum force production and rate of force development have been suggested as descending drive from supraspinal centers, spinal motoneuron excitability, and corticospinal inhibition of descending drive; all of which influence motor unit recruitment and/or firing rate. Resistance-trained Master athletes offer a good source of information regarding the inevitable effects of aging despite the countermeasure of systematic resistance-training. However, most evidence of neural adaptation is derived from longitudinal intervention studies in pre…

0301 basic medicineAgingmedicine.medical_treatmentCortical imagingBiochemistry0302 clinical medicineEndocrinologymotor unitvoimantuotto (fysiologia)motoneuroninterventionMotor NeuronsbiologyexercisekuntoliikuntaNeural adaptationinterventiotutkimusAdaptation PhysiologicalTranscranial Magnetic Stimulationmedicine.anatomical_structurehermo-lihastoimintaneuromuscularvoimaharjoittelustrengthRecruitment Neurophysiologicalmedicine.medical_specialty03 medical and health sciencesPhysical medicine and rehabilitationGood evidenceGeneticsmedicineHumansMuscle SkeletalMolecular BiologyAgedAthletesbusiness.industryElectromyographyagingResistance trainingResistance TrainingCell Biologybiology.organism_classificationMotor unitTranscranial magnetic stimulation030104 developmental biologyikääntyminenMotor unit recruitmentbusiness030217 neurology & neurosurgerylihasvoima
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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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Neuronal LRP4 regulates synapse formation in the developing CNS

2017

The low-density lipoprotein receptor-related protein 4 (LRP4) is essential in muscle fibers for the establishment of the neuromuscular junction. Here, we show that LRP4 is also expressed by embryonic cortical and hippocampal neurons, and that downregulation of LRP4 in these neurons causes a reduction in density of synapses and number of primary dendrites. Accordingly, overexpression of LRP4 in cultured neurons had the opposite effect inducing more but shorter primary dendrites with an increased number of spines. Transsynaptic tracing mediated by rabies virus revealed a reduced number of neurons presynaptic to the cortical neurons in which LRP4 was knocked down. Moreover, neuron-specific kno…

0301 basic medicineDendritic spineRabiesSynaptogenesisHippocampusBiologyHippocampal formationHippocampusNeuromuscular junctionGene Knockout TechniquesMice03 medical and health sciences0302 clinical medicinemedicineAnimalsLrp4 ; Central Nervous System Development ; Synapse Formation ; Dendritogenesis ; Transsynaptic Tracing ; Agrin ; In Utero Electroporation ; Psd95 ; Bassoon ; MouseMolecular BiologyCells CulturedLDL-Receptor Related ProteinsCerebral CortexGene knockdownAgrinDendritesCortex (botany)Cell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureReceptors LDLnervous systemRabies virusSynapsesImmunology030217 neurology & neurosurgeryDevelopmental Biology
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The neurochaperonopathies: Anomalies of the chaperone system with pathogenic effects in neurodegenerative and neuromuscular disorders

2021

The chaperone (or chaperoning) system (CS) constitutes molecular chaperones, co-chaperones, and chaperone co-factors, interactors and receptors, and its canonical role is protein quality control. A malfunction of the CS may cause diseases, known as the chaperonopathies. These are caused by qualitatively and/or quantitatively abnormal molecular chaperones. Since the CS is ubiquitous, chaperonopathies are systemic, affecting various tissues and organs, playing an etiologic-pathogenic role in diverse conditions. In this review, we focus on chaperonopathies involved in the pathogenic mechanisms of diseases of the central and peripheral nervous systems: the neurochaperonopathies (NCPs). Genetic …

0301 basic medicineHspsDiseasechaperonopathieslcsh:Technologylcsh:Chemistry03 medical and health sciences0302 clinical medicineneurochaperonopathieschaperone systemchaperonotherapy.medicineGeneral Materials ScienceReceptorInstrumentationGenelcsh:QH301-705.5Fluid Flow and Transfer Processesbiologylcsh:TSettore BIO/16 - Anatomia UmanaProcess Chemistry and TechnologyNeurodegenerationmolecular chaperonesnervous systemGeneral Engineeringmedicine.diseaseHsp90lcsh:QC1-999Computer Science ApplicationsCell biologyPatient management030104 developmental biologylcsh:Biology (General)lcsh:QD1-999lcsh:TA1-2040Chaperone (protein)biology.proteinChaperone system ChaperonopathiesChaperonotherapy Hsps Molecular chaperones Nervous system Neurochaperonopathies Neurodegeneration neuromuscular disorderHSP60lcsh:Engineering (General). Civil engineering (General)030217 neurology & neurosurgerylcsh:Physics
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An Integrated Pharmacophore/Docking/3D-QSAR Approach to Screening a Large Library of Products in Search of Future Botulinum Neurotoxin A Inhibitors

2020

Botulinum toxins are neurotoxins produced by Clostridium botulinum. This toxin can be lethal for humans as a cause of botulism

0301 basic medicineModels MolecularBotulinum ToxinsDatabases FactualNeuromuscular transmissionQuantitative Structure-Activity RelationshipPharmacologymedicine.disease_cause01 natural sciencesType Alcsh:ChemistryModelsClostridium botulinumbotulinum neurotoxin ABotulismBotulinum Toxins Type Alcsh:QH301-705.5Spectroscopyfood and beveragesGeneral MedicineBotulinum neurotoxinComputer Science ApplicationsdockingPharmacophoreQuantitative structure–activity relationshipStatic ElectricityChemicalbotulinum neurotoxin A virtual screening docking 3D-QSAR molecular dynamicsMolecular Dynamics SimulationArticleCatalysisInorganic ChemistrySmall Molecule Libraries03 medical and health sciencesDatabasesmedicinePhysical and Theoretical ChemistryMolecular BiologyFactual3D-QSARVirtual screening010405 organic chemistrybusiness.industryfungiOrganic ChemistryMolecularHydrogen Bondingmedicine.diseasevirtual screeningmolecular dynamics0104 chemical sciences030104 developmental biologyModels Chemicallcsh:Biology (General)lcsh:QD1-999Docking (molecular)Clostridium botulinumbusinessInternational Journal of Molecular Sciences
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Profilin 1 delivery tunes cytoskeletal dynamics toward CNS axon regeneration

2020

After trauma, regeneration of adult CNS axons is abortive, causing devastating neurologic deficits. Despite progress in rehabilitative care, there is no effective treatment that stimulates axonal growth following injury. Using models with different regenerative capacities, followed by gain- and loss-of-function analysis, we identified profilin 1 (Pfn1) as a coordinator of actin and microtubules (MTs), powering axonal growth and regeneration. In growth cones, Pfn1 increased actin retrograde flow, MT growth speed, and invasion of filopodia by MTs, orchestrating cytoskeletal dynamics toward axonal growth. In vitro, active Pfn1 promoted MT growth in a formin-dependent manner, whereas localizati…

0301 basic medicineNervous systemGrowth ConesNeuromuscular Junctionmacromolecular substancesGlial scar03 medical and health sciencesMiceProfilins0302 clinical medicineTransduction GeneticmedicineAnimalsAxonGrowth coneCytoskeletonSpinal Cord InjuriesMice KnockoutbiologyRegeneration (biology)General MedicineGenetic TherapyDependovirusSciatic NerveCell biologyNerve Regeneration030104 developmental biologymedicine.anatomical_structurenervous system030220 oncology & carcinogenesisForminsbiology.proteinSciatic nerveFilopodiaResearch Article
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Protein misfolding, amyotrophic lateral sclerosis and guanabenz: Protocol for a phase II RCT with futility design (ProMISe trial)

2017

IntroductionRecent studies suggest that endoplasmic reticulum stress may play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS) through an altered regulation of the proteostasis, the cellular pathway-balancing protein synthesis and degradation. A key mechanism is thought to be the dephosphorylation of eIF2α, a factor involved in the initiation of protein translation. Guanabenz is an alpha-2-adrenergic receptor agonist safely used in past to treat mild hypertension and is now an orphan drug. A pharmacological action recently discovered is its ability to modulate the synthesis of proteins by the activation of translational factors preventing misfolded protein accumula…

0301 basic medicineOncologyPathologyamyotrophic lateral sclerosisamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; adrenergic alpha-2 receptor agonist s; age of onset; amyotrophic lateral sclerosis; disease progression; double-blind method; endoplasmic reticulum stress; guanabenz; humans; italy; medical futility; neuroprotective agents; proteostasis deficienciesamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Medicine (all)randomized clinical trial guanabenzHelsinki declaration0302 clinical medicineProtocolAdrenergic alpha-2 Receptor Agonists1506Amyotrophic lateral sclerosisAge of OnsetGuanabenzMedicine (all)amyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein responseNeurodegenerationamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response;amyotrophic lateral sclerosis; guanabenz; motor neurone disease; neuromuscular disease; randomized clinical trial; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis DeficienciesGeneral Medicineunfolded protein responseEndoplasmic Reticulum StressRiluzoleNeuroprotective AgentsNeurologyTolerabilityItalyDisease Progression1713GuanabenzMedical Futilitymedicine.drugmedicine.medical_specialtyamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis Deficiencies; Medicine (all)Neuroprotection03 medical and health sciencesmotor neurone diseaseDouble-Blind MethodInternal medicinemedicineHumansProteostasis Deficienciesbusiness.industryAmbientaleneuromuscular diseaserandomized clinical trialmedicine.diseaseClinical trial030104 developmental biologybusiness030217 neurology & neurosurgery
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Small RNA-seq analysis of circulating miRNAs to identify phenotypic variability in Friedreich's ataxia patients.

2018

AbstractFriedreich’s ataxia (FRDA; OMIM 229300), an autosomal recessive neurodegenerative mitochondrial disease, is the most prevalent hereditary ataxia. In addition, FRDA patients have shown additional non-neurological features such as scoliosis, diabetes, and cardiac complications. Hypertrophic cardiomyopathy, which is found in two thirds of patients at the time of diagnosis, is the primary cause of death in these patients. Here, we used small RNA-seq of microRNAs (miRNAs) purified from plasma samples of FRDA patients and controls. Furthermore, we present the rationale, experimental methodology, and analytical procedures for dataset analysis. This dataset will facilitate the identificatio…

0301 basic medicineStatistics and ProbabilityEpigenomicsSmall RNAData DescriptorAtaxiaMitochondrial diseaseLibrary and Information SciencesBioinformaticsEducation03 medical and health sciences0302 clinical medicinemicroRNAMedicineHumansCirculating MicroRNAPathologicalCause of deathbusiness.industrySequence Analysis RNAHypertrophic cardiomyopathyNeuromuscular diseasemedicine.diseasePhenotypeComputer Science Applications030104 developmental biologyFriedreich AtaxiaNext-generation sequencingmedicine.symptomStatistics Probability and Uncertaintybusiness030217 neurology & neurosurgeryInformation SystemsScientific data
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The Amino Acid Transporter JhI-21 Coevolves with Glutamate Receptors, Impacts NMJ Physiology, and Influences Locomotor Activity in Drosophila Larvae

2015

AbstractChanges in synaptic physiology underlie neuronal network plasticity and behavioral phenomena, which are adjusted during development. The Drosophila larval glutamatergic neuromuscular junction (NMJ) represents a powerful synaptic model to investigate factors impacting these processes. Amino acids such as glutamate have been shown to regulate Drosophila NMJ physiology by modulating the clustering of postsynaptic glutamate receptors and thereby regulating the strength of signal transmission from the motor neuron to the muscle cell. To identify amino acid transporters impacting glutmatergic signal transmission, we used Evolutionary Rate Covariation (ERC), a recently developed bioinforma…

0301 basic medicinejuvenile-hormonemelanogasterAmino Acid Transport Systemsextracellular glutamateprotein-protein interactionsPhysiology[ SDV.BA ] Life Sciences [q-bio]/Animal biologySynaptic Transmissionin-vivo0302 clinical medicinePostsynaptic potentialDrosophila Proteinsgenesglial xctMotor NeuronsAnimal biologyMultidisciplinary[SDV.BA]Life Sciences [q-bio]/Animal biologyGlutamate receptorBiological Evolutiondrosophilemedicine.anatomical_structureReceptors GlutamateLarvaExcitatory postsynaptic potentialDrosophila[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Drosophila ProteinSignal Transductionevolutionary rate covariationNeuromuscular JunctionPresynaptic TerminalsNeurotransmissionBiologyMotor ActivityArticlesynaptic vesicle03 medical and health sciencesGlutamatergicneuromuscular-junctionBiologie animalemedicineAnimalsAmino acid transporterevolutionary rate covariation;protein-protein interactions;juvenile-hormone;neuromuscular-junction;synaptic vesicle;in-vivo;extracellular glutamate;glial xct;melanogaster;genesfungiNeurosciencesExcitatory Postsynaptic PotentialsMotor neuron030104 developmental biology[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neurons and CognitionMutation030217 neurology & neurosurgeryScientific Reports
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Corticoperipheral neuromuscular disconnection in obstructive sleep apnoea.

2020

Abstract The roles of central nervous mechanisms and cortical output in obstructive sleep apnoea remain unclear. We addressed corticomuscular coupling between cortical sensorimotor areas and lower facial motor units as a mechanistic pathway and as a possible surrogate marker of corticoperipheral motor control in obstructive sleep apnoea. In this exploratory cross-sectional retrospective study, we analysed EEG (C3 and C4 leads) and chin EMG from polysomnography recordings in 86 participants (22 females; age range: 26–81 years): 27 with mild (respiratory disturbance index = 5–15 events/h), 21 with moderate (15–30 events/h) and 23 with severe obstructive sleep apnoea (>30 events/h) and 15 cont…

0301 basic medicinemedicine.medical_specialtyobstructive sleep apnoeacorticalPolysomnography03 medical and health sciences0302 clinical medicineInternal medicineRespiratory disturbance indexmedicinecouplingSleep Stagesmedicine.diagnostic_testbusiness.industryGeneral EngineeringMotor controlmedicine.diseasemotorMotor unitObstructive sleep apneaAutonomic nervous system030104 developmental biologyBreathingCardiologyOriginal Articleneuromuscularbusiness030217 neurology & neurosurgeryBrain communications
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