Search results for "neuronal damage"

showing 7 items of 7 documents

Serum neurofilament light chain is a biomarker of acute and chronic neuronal damage in early multiple sclerosis.

2018

Background: Monitoring neuronal injury remains one key challenge in early relapsing-remitting multiple sclerosis (RRMS) patients. Upon axonal damage, neurofilament – a major component of the neuro-axonal cytoskeleton – is released into the cerebrospinal fluid (CSF) and subsequently peripheral blood. Objective: To investigate the relevance of serum neurofilament light chain (sNfL) for acute and chronic axonal damage in early RRMS. Methods: sNfL levels were determined in 74 patients (63 therapy-naive) with recently diagnosed clinically isolated syndrome (CIS) or RRMS using Single Molecule Array technology. Standardized 3 T magnetic resonance imaging (MRI) was performed at baseline and 1–3 con…

AdultMalePathologymedicine.medical_specialtyNeurofilamentMultiple SclerosisNeurofilament lightIntermediate FilamentsSeverity of Illness IndexDisease activity03 medical and health sciencesYoung Adult0302 clinical medicineNeuronal damageNeurofilament ProteinsMedicineHumans030212 general & internal medicineNeuronsbusiness.industryMultiple sclerosisNeurodegenerationBrainMiddle Agedmedicine.diseaseNeurologyBiomarker (medicine)FemaleNeurology (clinical)Atrophybusiness030217 neurology & neurosurgeryClinical progressionBiomarkersMultiple sclerosis (Houndmills, Basingstoke, England)
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB(1)).

2012

Endocannabinoids exert numerous effects in the CNS under physiological and pathological conditions. The aim of the present study was to examine whether the endocannabinoid N-arachidonoyldopamine (NADA) may protect neurons in excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). OHSC were excitotoxically lesioned by application of N-methyl-d-aspartate (NMDA, 50 μM) for 4 h and subsequently treated with different NADA concentrations (0.1 pM-50 μM) alone or in combination with cannabinoid receptor antagonists. NADA protected dentate gyrus granule cells and caused a slight reduction in the number of microglial cells. The number of degenerated neurons significantly decreased be…

Cannabinoid receptorDopamineTRPV1Arachidonic AcidsPharmacologyNeuroprotectionHippocampusCellular and Molecular NeuroscienceMicePiperidinesReceptor Cannabinoid CB1Neuronal damageAnimalsRats WistarCells CulturedPharmacologyNeuronsChemistryDentate gyrusExcitatory Postsynaptic PotentialsEndocannabinoid systemRatsNeuroprotective Agentsnervous systemNerve DegenerationCannabinoid receptor antagonistNMDA receptorPyrazolesNeuropharmacology
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Refuting the challenges of the developmental shift of polarity of GABA actions: GABA more exciting than ever!

2012

International audience; During brain development, there is a progressive reduction of intracellular chloride associated with a shift in GABA polarity: GABA depolarizes and occasionally excites immature neurons, subsequently hyperpolarizing them at later stages of development. This sequence, which has been observed in a wide range of animal species, brain structures and preparations, is thought to play an important role in activity-dependent formation and modulation of functional circuits. This sequence has also been considerably reinforced recently with new data pointing to an evolutionary preserved rule. In a recent ``Hypothesis and Theory Article,'' the excitatory action of GABA in early …

GABA; giant depolarizing potentials; energy substrates; brain slices; chloride homeostasis; developmentBrain developmentchloride homeostasisPolarity (physics)energy substratesBiologylcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceGABA0302 clinical medicineGiant depolarizing potentialsNeuronal damageAnimal speciesDevelopmental neurobiologybooklcsh:Neurosciences. Biological psychiatry. Neuropsychiatrydevelopment030304 developmental biology0303 health sciencesbrain slicesHypothesis and Theory Articledevelopment.Excitatory postsynaptic potentialbook.journal[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]giant depolarizing potentialsNeuroscience030217 neurology & neurosurgeryNeuroscience
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Glial Protection Against Neuronal Damage

1997

Glial homeostatic mechanisms are involved in neuronal protection during the early phase of cerebral ischemia. These protective effects include, among others, glutamate uptake and the regulation of pH in the extracellular space of the brain. Uptake of glutamate goes along with glial swelling, as does the elimination of protons from the glial cytosol. Five transport systems interact in order to maintain a normal intra- and extracellular pH in the brain.

Glutamate uptakeCytosolnervous systemChemistryNeuronal damageIschemiamedicineGlutamate receptorExtracellularNeuronal protectionmedicine.diseaseHomeostasisCell biology
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Identification of inflammatory neuronal injury and prevention of neuronal damage in multiple sclerosis: hope for novel therapies?

2013

Importance Although multiple sclerosis (MS) has long been considered the prototype for an inflammatory, demyelinating disease of the central nervous system, modern histopathology and imaging techniques show that significant damage to neuronal structures already start occurring in the earliest stages of the disease. As the disease progresses, the extent of neuronal pathology accumulates. Therapeutic progress in terms of the prevention of increased disability has only just begun. Objective To review possible diagnostic improvements of neuronal compartment pathology as well as direct therapeutic interventions based on reports from the last decade and outline clinical results from studies and p…

NeuronsMultiple Sclerosisbusiness.industryMultiple sclerosisCentral nervous systemAnti-Inflammatory AgentsDiseasemedicine.diseaseNeuroprotectionClinical trialmedicine.anatomical_structureNeuronal damageNerve DegenerationDemyelinating diseasemedicineDisease ProgressionHumansIdentification (biology)Neurology (clinical)businessNeuroscienceJAMA neurology
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Multiple Sclerosis Therapy Consensus Group (MSTCG): position statement on disease-modifying therapies for multiple sclerosis (white paper)

2021

Multiple sclerosis is a complex, autoimmune-mediated disease of the central nervous system characterized by inflammatory demyelination and axonal/neuronal damage. The approval of various disease-modifying therapies and our increased understanding of disease mechanisms and evolution in recent years have significantly changed the prognosis and course of the disease. This update of the Multiple Sclerosis Therapy Consensus Group treatment recommendation focuses on the most important recommendations for disease-modifying therapies of multiple sclerosis in 2021. Our recommendations are based on current scientific evidence and apply to those medications approved in wide parts of Europe, particular…

Position statementmedicine.medical_specialtytreatment recommendationMedizin610 Medicine & healthReviewDiseasemultiple sclerosis03 medical and health sciences0302 clinical medicineWhite paperNeuronal damagemedicine030212 general & internal medicineRC346-429610 Medicine & healthIntensive care medicinePharmacologybusiness.industryMultiple sclerosisDisease mechanismsGuidelinemedicine.diseasedisease-modifying therapy3. Good healthGroup treatmentNeurologyNeurology. Diseases of the nervous systemNeurology (clinical)businessguideline030217 neurology & neurosurgeryTherapeutic Advances in Neurological Disorders
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Effect of the serum from multiple sclerosis patients on an in vitro model of blood-brain barrier.

2008

Multiple sclerosis (MS) is characterized by focal inflammatory demyelination, largely due to autoimmune responses against different components of the myelin sheet. It is also generally accepted that the pathogenesis of MS consists of inflammatory and neurodegenerative phases, where demyelination should produce partially reversible clinical deficits that can remit, due to limited remyelination, while axonal degeneration produces permanent non-remitting clinical damage. It is also assumed that nervous system inflammation is initiated by autoreactive, myelin-specific T cells that permeate the blood-brain barrier and trigger a series of events leading to tissue destruction. In addition to antib…

multiple sclerosiin vitro modelSettore BIO/10 - Biochimicaneuronal damageblood-brain barrierbrain cell culture
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