Search results for "Amy"

showing 10 items of 1486 documents

The Microbiota Promotes Arterial Thrombosis in Low-Density Lipoprotein Receptor-Deficient Mice

2019

Our results demonstrate a functional role for the commensal microbiota in atherothrombosis. In a ferric chloride injury model of the carotid artery, GF C57BL/6J mice had increased occlusion times compared to colonized controls. Interestingly, in late atherosclerosis, HFD-fed GF Ldlr−/− mice had reduced plaque rupture-induced thrombus growth in the carotid artery and diminished ex vivo thrombus formation under arterial flow conditions.

Male0209 industrial biotechnologyVery low-density lipoproteinChemokine CXCL102 engineering and technology030204 cardiovascular system & hematologyarterial thrombosisApplied Microbiology and BiotechnologyACTIVATIONMicechemistry.chemical_compound020901 industrial engineering & automation0302 clinical medicinegermfree0202 electrical engineering electronic engineering information engineeringMedicinevascular inflammationPlateletChemokine CCL7lcsh:QH301-705.5platelet0303 health sciencesatherosclerosis mouse modelsfood and beveragesThrombosisPlaque AtheroscleroticQR1-502late atherosclerosis3. Good healthHolobiontlow-density lipoprotein receptorgerm-freeplateletscardiovascular systemFemalelipids (amino acids peptides and proteins)GLYCOPROTEIN-VIBlood streamResearch ArticleRECRUITMENTmedicine.medical_specialtyNutritional compositionCOAGULATION610 Medicine & healthBiologyMETABOLISMBiochemistry Genetics and Molecular Biology (miscellaneous)MicrobiologyMicrobiologyHost-Microbe BiologyProinflammatory cytokinePLATELET HYPERREACTIVITY03 medical and health sciencesINFLAMMATIONVirologyInternal medicineatherothrombosisGeneticsmicrobiotaAnimalsInterleukin 9Platelet activationcardiovascular diseasesThrombusMolecular Biology030304 developmental biologygut microbiotabusiness.industryCholesterolcarotid artery020208 electrical & electronic engineeringcholesterolnutritional and metabolic diseasesCell Biologymedicine.diseaseMicroreviewCHLAMYDIA-PNEUMONIAEMice Mutant StrainsGastrointestinal MicrobiomeEndocrinologyReceptors LDLlcsh:Biology (General)chemistryArterial thrombusLDL receptorParasitologyatherosclerosisbusinessEx vivoLipoproteinmBio
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Reduced firing rates of pyramidal cells in the frontal cortex of APP/PS1 can be restored by acute treatment with levetiracetam

2020

Contains fulltext : 229488.pdf (Publisher’s version ) (Open Access) Contains fulltext : 229488pre.pdf (Author’s version preprint ) (Open Access) In recent years, aberrant neural oscillations in various cortical areas have emerged as a common physiological hallmark across mouse models of amyloid pathology and patients with Alzheimer's disease. However, much less is known about the underlying effect of amyloid pathology on single cell activity. Here, we used high-density silicon probe recordings from frontal cortex area of 9-month-old APP/PS1 mice to show that local field potential power in the theta and beta band is increased in transgenic animals, whereas single-cell firing rates, specifica…

Male0301 basic medicineAgingAlzheimer`s disease Donders Center for Medical Neuroscience [Radboudumc 1]LevetiracetamAction PotentialsamyloidoosiLocal field potentialAlzheimerin tautiAmyloid beta-Protein Precursor0302 clinical medicineBeta RhythmChemistryPyramidal CellsGeneral Neuroscienceamyloidfood and beveragesAmyloidosisPhenotypePathophysiologyFrontal Lobesingle cellmedicine.anatomical_structureLevetiracetamPyramidal cellAlzheimer’s diseasemedicine.drugNeuroinformaticspatofysiologiaAmyloidmouse modelTransgeneMice Transgenic03 medical and health sciencesAlzheimer Diseasemental disordersPresenilin-1medicineAnimalslocal field potential (LFP)hermosolutDisease Models Animal030104 developmental biologynervous systemfiring rateNeurology (clinical)Geriatrics and GerontologyNeuroscience030217 neurology & neurosurgeryDevelopmental BiologyNeurobiology of Aging
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ATNX2 is not a regulatory gene in Italian amyotrophic lateral sclerosis patients with C9ORF72 GGGGCC expansion

2015

Abstract There are indications that both familial amyotrophic lateral sclerosis (ALS) and sporadic ALS phenotype and prognosis are partly regulated by genetic and environmental factors, supporting the theory that ALS is a multifactorial disease. The aim of this article was to assess the role of ATXN2 intermediate length repeats in a large series of Italian and Sardinian ALS patients and controls carrying a pathogenetic C9ORF72 GGGGCC hexanucleotide repeat. A total of 1972 ALS cases were identified through the database of the Italian ALS Genetic consortium, a collaborative effort including 18 ALS centers throughout Italy. The study population included: (1) 276 Italian and 57 Sardinian ALS ca…

Male0301 basic medicineAgingC9ORF72Genetic Association Studie030105 genetics & heredityBiologySettore MED/03 - GENETICA MEDICA03 medical and health sciences0302 clinical medicineC9orf72medicineAlleleAmyotrophic lateral sclerosisAmyotrophic lateral sclerosiAgedAtaxin-2Regulator geneAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neuroscience (all); Medicine (all); Aging; Developmental Biology; Geriatrics and Gerontology; Neurology (clinical)GeneticsDNA Repeat ExpansionNeuroscience (all)ProteinMedicine (all)General NeuroscienceATXN2Middle AgedDNA Repeat Expansionmedicine.diseaseAmyotrophic lateral sclerosis3. Good healthC9orf72 ProteinAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyPhenotypeItalyPopulation studyFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyTrinucleotide repeat expansion030217 neurology & neurosurgeryHumanDevelopmental Biology
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Garcinoic acid prevents β-amyloid (Aβ) deposition in the mouse brain

2020

Garcinoic acid (GA or δ-T3-13'COOH), is a natural vitamin E metabolite that has preliminarily been identified as a modulator of nuclear receptors involved in β-amyloid (Aβ) metabolism and progression of Alzheimer's disease (AD). In this study, we investigated GA's effects on Aβ oligomer formation and deposition. Specifically, we compared them with those of other vitamin E analogs and the soy isoflavone genistein, a natural agonist of peroxisome proliferator–activated receptor γ (PPARγ) that has therapeutic potential for managing AD. GA significantly reduced Aβ aggregation and accumulation in mouse cortical astrocytes. Similarly to genistein, GA up-regulated PPARγ expression and apolipoprote…

Male0301 basic medicineApolipoprotein EBiologiamedicine.medical_treatmentMetaboliteGenisteinFisiologiavitamin EPharmacologyProtein Aggregation PathologicalBiochemistry)protein aggregationgenisteinMiceProtein Aggregates03 medical and health scienceschemistry.chemical_compoundperoxisome proliferator-activated receptor gamma (PPARγ)neurodegenerative diseaseNeurobiologygarcinoic acidmedicineAnimalsBenzopyranstocotrienolReceptorMolecular BiologyPregnane X receptorAmyloid beta-Peptidespregnane X receptor (PXR)peroxisome proliferator-activated receptor (PPAR)030102 biochemistry & molecular biologyVitamin EBrainCell BiologyAlzheimer's diseasetocopherol030104 developmental biologyNuclear receptorchemistryperoxisome proliferator-activated receptor gamma (PPAR gamma)amyloid-beta (AB)apolipoprotein E (ApoETocotrienolAlzheimer diseaseapolipoprotein E (ApoE)
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Disruption of the ATXN1-CIC complex causes a spectrum of neurobehavioral phenotypes in mice and humans

2017

International audience; Gain-of-function mutations in some genes underlie neurodegenerative conditions, whereas loss-of-function mutations in the same genes have distinct phenotypes. This appears to be the case with the protein ataxin 1 (ATXN1), which forms a transcriptional repressor complex with capicua (CIC). Gain of function of the complex leads to neurodegeneration, but ATXN1-CIC is also essential for survival. We set out to understand the functions of the ATXN1-CIC complex in the developing forebrain and found that losing this complex results in hyperactivity, impaired learning and memory, and abnormal maturation and maintenance of upper-layer cortical neurons. We also found that CIC …

Male0301 basic medicineAutism Spectrum DisorderAtaxin 1neuronsautismNerve Tissue Proteinsattention-deficit/hyperactivity disorderAmygdalaArticleMice03 medical and health sciencesTranscriptional repressor complexataxin-1Cerebellum[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineAnimalsHumansAttention deficit hyperactivity disorderInterpersonal Relationssca1 neuropathologybiologysocial-behaviorNeurodegenerationcag repeatNuclear ProteinsNeurodegenerative Diseasesmedicine.diseasePhenotypeRepressor ProteinsPhenotype030104 developmental biologymedicine.anatomical_structureAutism spectrum disorderintellectual disabilitybiology.proteinAutismFemaleNeurosciencetime pcr datarepressor capicua[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Memory-enhancing and brain protein expression-stimulating effects of novel calcium antagonist in Alzheimer’s disease transgenic female mice

2016

The prevalence of Alzheimer's disease (AD) is higher in females than in males, and causes more severe cognitive, memory and behavioral impairments. Previously, in male transgenic (Tg) APPSweDI mice, we reported that the novel lipophilic 1,4-dihydropyridine (DHP) derivative AP-12 crossed the blood-brain barrier, blocked neuronal and vascular calcium channels, changed brain protein expression and improved behavior. In this study, we used female Tg APPSweDI mice to assess the effects of AP-12 on behavior, and brain protein expression, with a particular focus on those of the GABAergic system. The results showed that in female Tg mice, similar to male Tg mice, AP-12 improved spatial learning/mem…

Male0301 basic medicineCingulate cortexDihydropyridinesmedicine.medical_specialtyElevated plus mazeVesicular Inhibitory Amino Acid Transport ProteinsHippocampusMice TransgenicWater mazeBiologyHippocampal formationGyrus CinguliHippocampusArticleAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineAlzheimer DiseaseMemoryInternal medicineNeuroplasticitymedicineAnimalsGABAergic NeuronsMaze LearningPharmacologyAmyloid beta-PeptidesNeuronal PlasticityGlutamate DecarboxylaseCalcium Channel BlockersUp-RegulationDisease Models Animal030104 developmental biologyEndocrinologyAnti-Anxiety AgentsBlood-Brain BarrierSynaptic plasticityGABAergicCalciumFemale030217 neurology & neurosurgeryPharmacological Research
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Early life stress is a risk factor for excessive alcohol drinking and impulsivity in adults and is mediated via a CRF/GABAA mechanism

2016

Childhood stress and trauma are associated with substance use disorders in adulthood, but the neurological changes that confer increased vulnerability are largely unknown. In this study, maternal separation (MS) stress, restricted to the pre-weaning period, was used as a model to study mechanisms of protracted effects of childhood stress/traumatic experiences on binge drinking and impulsivity. Using an operant self-administration model of binge drinking and a delay discounting assay to measure impulsive-like behavior, we report that early life stress due to MS facilitated acquisition of binge drinking and impulsivity during adulthood in rats. Previous studies have shown heightened levels of…

Male0301 basic medicineCorticotropin-Releasing HormonePhysiologySelf AdministrationRats Sprague-DawleyBehavioral Neuroscience0302 clinical medicineGABA receptorRisk FactorsAntalarminPrefrontal cortexGABAA receptorMaternal DeprivationAmygdalaVitamin B 12Psychiatry and Mental healthNeuropsychology and Physiological Psychologymedicine.anatomical_structureFemalemedicine.symptomPsychologymedicine.drugClinical psychologymedicine.medical_specialtyAlcohol Drinkingmedicine.drug_classPrefrontal CortexBinge drinkingImpulsivityReceptors Corticotropin-Releasing HormoneAmygdalaArticle03 medical and health sciencesInternal medicinemedicineAnimalsPyrrolesBenzodiazepineEthanolEndocrine and Autonomic SystemsReceptors GABA-ARatsPyrimidines030104 developmental biologyEndocrinologyImpulsive BehaviorConditioning OperantStress Psychological030217 neurology & neurosurgeryStress
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Effects of the Antidepressant Fluoxetine on the Somatostatin Interneurons in the Basolateral Amygdala

2018

Although the precise mechanism of action of antidepressant drugs remains elusive, the neuroplastic hypothesis has gained acceptance during the last two decades. Several studies have shown that treatment with antidepressants such as Fluoxetine is associated with enhanced plasticity in control animals, especially in regions such as the visual cortex, the hippocampus and the medial prefrontal cortex. More recently, the basolateral amygdala has been shown to be affected by Fluoxetine leading to a reopening of critical period-like plasticity in the fear and aggression circuits. One of the key elements triggering this type of brain plasticity are inhibitory networks, especially parvalbumin intern…

Male0301 basic medicineDendritic spinegenetic structuresInterneuronHippocampusMice TransgenicMice03 medical and health sciences0302 clinical medicineInterneuronsFluoxetineNeuroplasticitymedicineAnimalsPrefrontal cortexNeuronal PlasticitybiologyBasolateral Nuclear ComplexGeneral NeuroscienceAntidepressive Agents030104 developmental biologymedicine.anatomical_structureSomatostatinnervous systembiology.proteinSomatostatinNeuroscience030217 neurology & neurosurgeryParvalbuminBasolateral amygdalaNeuroscience
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Arachidonate 5-lipoxygenase (ALOX5) gene polymorphism is associated with Alzheimer's disease and body mass index

2016

IF 2.126; International audience; Dementias of old age, in particular Alzheimer's disease (AD), pose a growing threat to the longevity and quality of life of individuals as well as whole societies world-wide. The risk factors are both genetic and environmental (lifestyle) and there is an overlap with similar factors predisposing to cardiovascular diseases (CVD). Using a case control genetic approach, we have identified a SNP (rs10507391) in ALOX5 gene, previously associated with an increased risk of stroke, as a novel genetic risk factor for AD. ALOX5 gene encodes a 5'-lipoxygenase (5'-LO) activating protein (FLAP), a crucial component of the arachidonic acid/leukotriene inflammatory cascad…

Male0301 basic medicineDiseaseBioinformaticsBody Mass Index0302 clinical medicinePutative roleSurveys and QuestionnairesGenotypeMedicineCzech RepublicAged 80 and over2. Zero hungerGeneticsbiologyAlzheimer's disease3. Good healthRisk-factorsArachidonic acidNeurologyArachidonate 5-lipoxygenaseActivating proteinFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neuronal 5-LipoxygenaseLeukotrienesCurcuminGenotypeDna methylationFLAPPolymorphism Single NucleotideMouse modelAssociation03 medical and health sciencesMessenger-RnaAlzheimer DiseaseGeneticsHumansSNPPolymorphismSingle-Nucleotide polymorphisms5-lipoxygenase-activating proteinLife StyleGenetic Association StudiesAgedAmyloidotic phenotypeInflammationCaffeic acidArachidonate 5-Lipoxygenasebusiness.industryBody WeightOdds ratio030104 developmental biology[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Relative riskbiology.proteinNeurology (clinical)businessBody mass index030217 neurology & neurosurgeryJournal of the Neurological Sciences
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Role of Colchicine Treatment in Tumor Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS): Real-Life Data from the AIDA Network

2020

Objective. To analyze the potential role of colchicine monotherapy in patients with tumor necrosis factor receptor associated periodic syndrome (TRAPS) in terms of control of clinical and laboratory manifestations. Methods. Patients with TRAPS treated with colchicine monotherapy were retrospectively enrolled; demographic, clinical and therapeutic data were collected and statistically analysed after having clustered patients according to different times at disease onset, penetrance of mutations, dosage of colchicine, and different disease manifestations. Results. 24 patients (14 males; 15 with pediatric disease onset) treated with colchicine monotherapy were enrolled. Colchicine resulted in …

Male0301 basic medicineEye DiseasesTRAPSColchicineAIDA NetworkGene mutationGastroenterologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundSettore MED/38 - Pediatria Generale E Specialistica0302 clinical medicineReceptorsPathologyRB1-214ColchicineAge of OnsetYoung adultChildAmyloidosisAmyloidosisSyndromeMiddle AgedColchicine tumor necrosis factor TRAPSInflamacióPenetrancePhenotypeChild PreschoolFemaleJoint DiseasesResearch ArticleAdultRiskmedicine.medical_specialtyAdolescentFeverArticle SubjectImmunologyAdolescent; Adult; Age of Onset; Amyloidosis; Child; Child Preschool; Colchicine; Exanthema; Eye Diseases; Female; Fever; Humans; Joint Diseases; Male; Middle Aged; Mutation; Myalgia; Phenotype; Receptors Tumor Necrosis Factor; Retrospective Studies; Risk; Syndrome; Young AdultLower riskYoung Adult03 medical and health sciencesInternal medicinemedicineHumansPreschoolRetrospective StudiesInflammation030203 arthritis & rheumatologybusiness.industryTRAPSRetrospective cohort studyMyalgiaCell BiologyExanthemamedicine.disease030104 developmental biologychemistryMutationAge of onsetColchicineTumor Necrosis FactorbusinessMediators of Inflammation
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