Search results for "Neuron death"

showing 6 items of 6 documents

Therapeutic alternative of the ketogenic Mediterranean diet to improve mitochondrial activity in Amyotrophic Lateral Sclerosis (ALS): A Comprehensive…

2019

Abstract Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease which is pathogenically based on the mitochondrial alteration of motor neurons, causing progressive neuron death. While ALS is characterized by enormous oxidative stress, the Mediterranean diet has been seen to have high antioxidant power. Therefore, the aim of this study is to determine how the Mediterranean diet can improve mitochondrial activity, establishing the specific nutrients and, in addition, observing the pathogenic mechanisms related to the disease that would achieve this improvement. To this end, a comprehensive review of the literature was performed using PubMed. KBs have been observed to ha…

0301 basic medicineamyotrophic lateral sclerosismitochondria ; mediterranean diet ; amyotrophic lateral sclerosis ; ketone bodiesMediterranean dietReviewslcsh:TX341-641ReviewDiseaseMitochondrionBioinformaticsmedicine.disease_causeNeuroprotection03 medical and health sciences0302 clinical medicineKetogenesisMedicineAmyotrophic lateral sclerosisbusiness.industryfood and beveragesmediterranean dietmedicine.diseasemitochondria030104 developmental biologyketone bodiesbusinessNeuron deathlcsh:Nutrition. Foods and food supply030217 neurology & neurosurgeryOxidative stressFood ScienceFood Science & Nutrition
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Holo-APP and G-protein-mediated signaling are required for sAPPa-induced activation of the Akt survival pathway

2014

International audience; Accumulating evidence indicates that loss of physiologic amyloid precursor protein (APP) function leads to reduced neuronal plasticity, diminished synaptic signaling and enhanced susceptibility of neurons to cellular stress during brain aging. Here we investigated the neuroprotective function of the soluble APP ectodomain sAPPa (soluble APPa), which is generated by cleavage of APP by a-secretase along the non-amyloidogenic pathway. Recombinant sAPPa protected primary hippocampal neurons and SH-SY5Y neuroblastoma cells from cell death induced by trophic factor deprivation. We show that this protective effect is abrogated in neurons from APP-knockout animals and APP-de…

Cancer ResearchCell SurvivalADAM10Amino Acid MotifsImmunology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyIn Vitro TechniquesHydroxamic AcidsHippocampusNeuroprotectionCell LineADAM10 ProteinAmyloid beta-Protein PrecursorMicePhosphatidylinositol 3-Kinases03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemental disordersAmyloid precursor proteinAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase Inhibitors030304 developmental biologyMice Knockout0303 health sciencesbiologyBiochemistry and Molecular BiologyMembrane ProteinsDipeptidesCell BiologyMolecular biologyRecombinant ProteinsMice Inbred C57BLADAM ProteinsPertussis Toxinbiology.proteinOriginal ArticleSynaptic signalingAmyloid Precursor Protein SecretasesNeuron deathProto-Oncogene Proteins c-aktAmyloid precursor protein secretase030217 neurology & neurosurgeryBiokemi och molekylärbiologiSignal Transduction
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Sugammadex, a Neuromuscular Blockade Reversal Agent, Causes Neuronal Apoptosis in Primary Cultures

2013

Sugammadex, a γ-cyclodextrin that encapsulates selectively steroidal neuromuscular blocking agents, such as rocuronium or vecuronium, has changed the face of clinical neuromuscular pharmacology. Sugammadex allows a rapid reversal of muscle paralysis. Sugammadex appears to be safe and well tolerated. Its blood-brain barrier penetration is poor (< 3% in rats), and thus no relevant central nervous toxicity is expected. However the blood brain barrier permeability can be altered under different conditions (i.e. neurodegenerative diseases, trauma, ischemia, infections, or immature nervous system). Using MTT, confocal microscopy, caspase-3 activity, cholesterol quantification and Western-blot we …

Estrès oxidatiuSmac/Diablo and CASP-3.BiologyPharmacologymedicine.disease_causeSugammadexSugammadexAIFmedicineAnimalsRocuroniumCytCCells CulturedFisiologia cel·lularNeuronsNeuromuscular BlockadeapoptosisGeneral MedicineNeuromuscular Blocking AgentsRatsOxidative StressApoptosisAnesthesiaToxicityNeuromuscular BlockadeNeuron deathOxidative stressmedicine.drugResearch Papergamma-CyclodextrinsInternational Journal of Medical Sciences
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Overexpression of Septin 4, the Drosophila homologue of human CDCrel-1, is toxic for dopaminergic neurons

2007

parkin loss-of-function mutations are linked to autosomal recessive juvenile parkinsonism. Parkin is an E3 ubiquitin ligase that promotes degradation of specific target proteins by the proteasome. It has been proposed that loss of Parkin activity will result in accumulation of its substrates, thus leading to dopaminergic (DA) neuron death. In Drosophila, parkin mutations cause degeneration of a subset of DA neurons in the brain but no Parkin substrates have yet been described. Here we characterized the septin 4 gene, which encodes the Drosophila orthologue of human CDCrel-1, a Parkin substrate. We showed that Septin 4 overexpression causes age-dependent disruption of DA neuron integrity in …

GeneticsbiologyGeneral NeurosciencefungiMutantSeptinPhenotypeParkinnervous system diseasesUbiquitin ligaseCell biologymedicine.anatomical_structureProteasomebiology.proteinmedicineNeuronNeuron deathEuropean Journal of Neuroscience
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Relationship between within-host fitness and virulence in the vesicular stomatitis virus: correlation with partial decoupling.

2012

ABSTRACT Given the parasitic nature of viruses, it is sometimes assumed that rates of viral replication and dissemination within hosts (within-host fitness) correlate with virulence. However, there is currently little empirical evidence supporting this principle. To test this, we quantified the fitness and virulence of 21 single- or double-nucleotide mutants of the vesicular stomatitis virus in baby hamster kidney cells (BHK-21). We found that, overall, these two traits correlated positively, but significant outliers were identified. Particularly, a single mutation in the conserved C terminus of the N nucleocapsid (U1323A) had a strongly deleterious fitness effect but did not alter or even …

ImmunologyMutantVirulenceApoptosisBiologymedicine.disease_causeVirus ReplicationMicrobiologyVesicular stomatitis Indiana virusCell Line03 medical and health sciencesVesicular StomatitisMiceVirologyCricetinaemedicineBaby hamster kidney cellAnimals030304 developmental biologyGlycoproteinsGenetics0303 health sciencesMutationMice Inbred BALB CVirulence030302 biochemistry & molecular biologyCell MembraneBrainNucleocapsid Proteinsbiology.organism_classification3. Good healthProtein Structure TertiaryViral replicationGenetic Diversity and EvolutionVesicular stomatitis virusInsect ScienceMutationFemaleNeuron deathVesicular StomatitisJournal of virology
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Small Extracellular Vesicles Secreted by Region-specific Astrocytes Ameliorate the Mitochondrial Function in a Cellular Model of Parkinson’s Disease

2021

AbstractExtracellular vesicles (EVs) are emerging as powerful players in cell-to-cell communication both in health and diseased brain. In Parkinson’s disease (PD) – characterized by selective dopaminergic (DAergic) neuron death in ventral midbrain (VMB) and degeneration of DAergic terminals in striatum (STR) – astrocytes (AS) exert dual harmful/protective functions. When activated by chemokine CCL3, AS promote a robust DAergic neuroprotection both in cellular and pre-clinical models of PD, with mechanisms not fully elucidated. Here we used a combination of techniques to characterize AS-EVs derived from VMB and STR, and investigated their potential to exert neuroprotection. First, we show th…

Parkinson's diseaseChemistryDopaminergicmedicineSecretionStriatumCellular modelmedicine.disease_causeNeuron deathmedicine.diseaseNeuroprotectionOxidative stressCell biology
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