Search results for "Amy"

showing 10 items of 1486 documents

Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenot…

2021

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal lethality of germline knockout mice lacking the entire APP family has so far precluded the analysis of its physiological functions for the developing and adult brain. Here, we generated conditional APP/APLP1/APLP2 triple KO (cTKO) mice lacking the APP family in excitatory forebrain neurons from embryonic day 11.5 onwards. NexCre cTKO mice showed altered brain morphology with agenesis of the corpus callosum and disrupted hippocampal lamination. Further, NexCre cTKOs revealed reduced basal synaptic transmission and drastically reduced long-term potentiation that was associated with reduced dendritic length …

Male10017 Institute of AnatomyLong-Term PotentiationHippocampal formationSynaptic TransmissionAmyloid beta-Protein Precursor0302 clinical medicine2400 General Immunology and MicrobiologyAmyloid precursor proteinMolecular Biology of DiseaseAutism spectrum disorderMice KnockoutNeurons0303 health sciencesbiologyBehavior AnimalGeneral NeuroscienceBrain2800 General NeuroscienceLong-term potentiationArticlesPhenotype10076 Center for Integrative Human PhysiologyKnockout mouseFemalelearning and memory610 Medicine & healthGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesProsencephalon1300 General Biochemistry Genetics and Molecular Biologymental disorders1312 Molecular BiologyAnimalsLearningAPLP1Autistic DisorderSocial BehaviorMolecular BiologyAPLP2CA1 Region Hippocampal030304 developmental biologysynaptic plasticityGeneral Immunology and MicrobiologyAmyloid precursor proteinSynaptic plasticityForebrainSynapsesbiology.proteinAlzheimer570 Life sciences; biologyNeuroscience030217 neurology & neurosurgeryNeuroscienceThe EMBO journal
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18F-Florbetaben PET/CT to Assess Alzheimer's Disease: A new Analysis Method for Regional Amyloid Quantification.

2019

Background and purpose While AD can be definitively confirmed by postmortem histopathologic examination, in vivo imaging may improve the clinician's ability to identify AD at the earliest stage. The aim of the study was to test the performance of amyloid PET using new processing imaging algorithm for more precise diagnosis of AD. Methods Amyloid PET results using a new processing imaging algorithm (MRI-Less and AAL Atlas) were correlated with clinical, cognitive status, CSF analysis, and other imaging. The regional SUVR using the white matter of cerebellum as reference region and scores from clinical and cognitive tests were used to create ROC curves. Leave-one-out cross-validation was carr…

Male18F-florbetabenAmyloidSensitivity and SpecificityAmyloid-PET Imaging030218 nuclear medicine & medical imagingWhite matter03 medical and health sciences0302 clinical medicineAlzheimer DiseasePositron Emission Tomography Computed Tomographymental disordersStilbenesmedicineImage Processing Computer-AssistedDementiaHumansRadiology Nuclear Medicine and imaging18F-florbetaben; Alzheimer's disease; Amyloid-PET Imaging; MR-lessAgedRetrospective StudiesPET-CTAniline CompoundsReceiver operating characteristicbusiness.industry18F-florbetaben Alzheimer's disease Amyloid-PET Imaging MR-less Aged Alzheimer Disease Female Humans Image Processing Computer-Assisted Magnetic Resonance Imaging Male Positron Emission Tomography Computed Tomography Retrospective Studies Sensitivity and Specificity Aniline Compounds StilbenesAlzheimer's diseasemedicine.diseaseMagnetic Resonance Imagingmedicine.anatomical_structureMR-lessFemaleNeurology (clinical)Differential diagnosisNuclear medicinebusiness030217 neurology & neurosurgeryPreclinical imagingFrontotemporal dementiaJournal of neuroimaging : official journal of the American Society of Neuroimaging
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Predictors of non-invasive ventilation tolerance in amyotrophic lateral sclerosis

2011

Abstract Background The most frequent cause of death in patients with Amyotrophic Lateral Sclerosis (ALS) is respiratory failure. Recently, it has been shown that non-invasive ventilation improves survival and quality of life in ALS patients with respiratory failure, but little is known about predictors of non-invasive ventilation adaptation and tolerance. In this study we evaluated the effect of a comprehensive information about non-invasive ventilation use and a prolonged and intensive monitoring on tolerance to this palliative care. Methods We prospectively monitored all consecutive ALS patients with chronic respiratory failure and indication to non-invasive ventilation between January 2…

MaleALS Chronic respiratory failure Tolerance to non-invasive ventilation Bulbar impairment POSITIVE-PRESSURE VENTILATION QUALITY-OF-LIFE PRACTICE PARAMETER CARE MANAGEMENT STANDARDS BIPAPmedicine.medical_specialtyPalliative carePatientsTolerance to non-invasive ventilationBody Mass IndexQuality of lifeQUALITY-OF-LIFEPRACTICE PARAMETERMANAGEMENTHumansMedicineDementiaChronic respiratory failureOximetryProspective StudiesAmyotrophic lateral sclerosisIntensive care medicineBIPAPAgedCause of deathVentilators Mechanicaltolerancebusiness.industryAmyotrophic Lateral SclerosisRespiratory diseaseSialorrheaCAREMiddle Agedmedicine.diseaseRespiration ArtificialBulbar impairment POSITIVE-PRESSURE VENTILATIONCaregiversNeurologyRespiratory failureSpirometryChronic DiseaseNIVEmergency medicineBreathingFemaleSettore MED/26 - NeurologiaNeurology (clinical)Blood Gas AnalysisALSRespiratory InsufficiencybusinessSTANDARDSJournal of the Neurological Sciences
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Mycoplasma pneumoniae and Chlamydia pneumoniae infections in children with pneumonia. Mowgli Study Group.

2001

The most common clinical signs, host responses and radiographic patterns were studied in 203 Italian children hospitalized for community-acquired pneumonia in order to clarify the role of clinical and radiological characteristics in the diagnosis of Mycoplasma pneumoniae and/or Chlamydia pneumoniae infections. Antibody measurements in paired sera and polymerase chain reaction on nasopharyngeal aspirates were used to establish the diagnoses of acute. M. pneumoniae and C. pneumoniae infection, and the aetiologic data were correlated with the clinical, laboratory and radiographic data obtained on admission. No significant association was observed between evidence of M. pneumoniae and/or C. pne…

MaleAcute Disease; Pneumonia; Mycoplasma; Diagnosis; Differential; Humans; Nasopharynx; Child; Mycoplasma pneumoniae; Preschool; Polymerase Chain Reaction; Lung; Bacterial; Antibodies; Chlamydia Infections; Community-Acquired Infections; Chlamydophila pneumoniae; Adolescent; Male; FemaleAdolescentPolymerase Chain ReactionAntibodiesDiagnosis DifferentialMycoplasmachildrenChlamydia pneumoniaeNasopharynxDiagnosisPneumonia MycoplasmaPneumonia BacterialpneumoniaHumansPreschoolChildLungBacterialChlamydia InfectionsChlamydophila pneumoniaeAntibodies BacterialMycoplasma pneumoniaeCommunity-Acquired InfectionsRadiographyChild PreschoolDifferentialAcute DiseaseFemaleThe European respiratory journal
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Mutations in the Matrin 3 gene cause familial amyotrophic lateral sclerosis.

2013

MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Using exome sequencing, we identified mutations in MATR3 in ALS kindreds. We also observed MATR3 pathology in ALS-affected spinal cords with and without MATR3 mutations. Our data provide more evidence supporting the role of aberrant RNA processing in motor neuron degeneration. © 2014 Nature America, Inc. All rights reserved.

MaleAged Aged; 80 and over Amyotrophic Lateral Sclerosis; genetics/pathology Computational Biology DNA Mutational Analysis DNA-Binding Proteins; metabolism Family Health Female Genetic Predisposition to Disease; genetics Genotype Humans Male Middle Aged Muscle; Skeletal; metabolism/pathology Mutation; genetics Neurologic Examination Nuclear Matrix-Associated Proteins; genetics/metabolism RNA-Binding Proteins; genetics/metabolism Spinal Cord; metabolism/pathologyDNA Mutational Analysisgenetics/metabolismRNA-binding proteinSettore MED/03 - GENETICA MEDICAmedicine.disease_cause0302 clinical medicineNuclear Matrix-Associated ProteinsGenotype80 and overgeneticsAmyotrophic lateral sclerosisExome sequencingGeneticsAged 80 and overNeurologic Examination0303 health sciencesMutationGeneral NeuroscienceRNA-Binding ProteinsSkeletalMiddle AgedDNA-Binding ProteinsMATR3medicine.anatomical_structureSpinal Cordfamilial amyotrophic lateral sclerosisMuscleSettore MED/26 - NeurologiaFemaleFrontotemporal dementiametabolism/pathologyGenotypeArticle03 medical and health sciencesgenetics; familial amyotrophic lateral sclerosismental disordersmedicineHumansGenetic Predisposition to DiseaseMuscle Skeletal030304 developmental biologyAgedFamily Healthbusiness.industryAmyotrophic Lateral Sclerosisgenetics/pathologyRNAComputational BiologySpinal cordmedicine.diseaseMutationgeneticbusinessNeurosciencemetabolism030217 neurology & neurosurgery
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Altered insulin pathway compromises mitochondrial function and quality control both in in vitro and in vivo model systems.

2021

Abstract Altered insulin signaling and insulin resistance are considered the link between Alzheimer's disease (AD) and metabolic syndrome. Here, by using an in vitro and an in vivo model, we investigated the relationship between these disorders focusing on neuronal mitochondrial dysfunction and mitophagy. In vitro Aβ insult induced the opening of mitochondrial permeability transition pore (mPTP), mitochondrial membrane potential (ΔΨm) loss, and apoptosis while insulin addition ameliorated these dysfunctions. The same alterations were detected in a 16 weeks of age mouse model of diet-induced obesity and insulin resistance. In addition, we detected an increase of fission related proteins and …

MaleAgingAmyloid beta-Peptidemedicine.medical_treatmentMetabolic diseasePINK1Insulin pathway Neurodegeneration Metabolic diseases Mitochondrion Mitophagy AgingMitochondrionDiet High-FatParkinNOMiceInsulin resistanceMetabolic DiseasesCell Line TumorMitophagymedicineAnimalsHumansInsulinMitochondrionNeurodegenerationMolecular BiologyAmyloid beta-PeptidesbiologyAnimalChemistryInsulinMitophagyCell Biologymedicine.diseaseCell biologyMitochondriaMice Inbred C57BLInsulin receptorMitochondrial permeability transition porebiology.proteinMolecular MedicineInsulin ResistanceInsulin pathwayHumanSignal TransductionMitochondrion
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CHCH10 mutations in an Italian cohort of familial and sporadic amyotrophic lateral sclerosis patients

2015

Mutations in CHCHD10 have recently been described as a cause of frontotemporal dementia (FTD) comorbid with amyotrophic lateral sclerosis (ALS). The aim of this study was to assess the frequency and clinical characteristics of CHCHD10 mutations in Italian patients diagnosed with familial (n= 64) and apparently sporadic ALS (n= 224). Three apparently sporadic patients were found to carry c.100C>T (p.Pro34Ser) heterozygous variant in the exon 2 of CHCHD10. This mutation had been previously described in 2 unrelated French patients with FTD-ALS. However, our patients had a typical ALS, without evidence of FTD, cerebellar or extrapyramidal signs, or sensorineural deficits. We confirm that CHC…

MaleAgingPediatricsmedicine.medical_specialtyPathologyAmyotrophic lateral sclerosis; CHCHD10; Familial; Sporadic; Aged; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Frontotemporal Dementia; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Mitochondrial Proteins; Genetic Association Studies; MutationGenetic Association StudieDiseaseSettore MED/03 - GENETICA MEDICAmedicine.disease_causeCohort StudiesMitochondrial ProteinsExonFamilialmental disordersmedicineHumansMitochondrial ProteinDementiaGenetic Predisposition to DiseaseAmyotrophic lateral sclerosisAmyotrophic lateral sclerosis; CHCHD10; Familial; Sporadic; Aged; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Frontotemporal Dementia; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Mitochondrial Proteins; Genetic Association Studies; Mutation; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyGenetic Association StudiesAmyotrophic lateral sclerosiAgedMutationNeuroscience (all)business.industryGeneral NeuroscienceMiddle AgedAmyotrophic lateral sclerosisSporadicmedicine.disease3. Good healthAmyotrophic lateral sclerosis; CHCHD10; Familial; SporadicCHCHD10ItalyFrontotemporal DementiaMutationCohortFemaleNeurology (clinical)Cohort StudieGeriatrics and GerontologybusinessHumanDevelopmental BiologyFrontotemporal dementiaCohort studyNeurobiology of Aging
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FUS MUTATIONS IN SPORADIC AMYOTROPHIC LATERAL SCLEROSIS: CLINICAL AND GENETIC ANALYSIS

2012

Fused in sarcoma (FUS) or translocation in liposarcoma (TLS), a DNA/RNA-binding protein, causes a dominant autosomal inherited form of amyotrophic lateral sclerosis (ALS), ALS 6. Its main role in neurodegeneration is highlighted by the presence of cytoplasmic accumulation of its mutant protein form in ALS patients. To further define the frequency and spectrum of FUS gene mutations, we have performed a molecular screening of a cohort of 327 Italian patients from Southern Italy with sporadic ALS (SALS). We identified 4 patients carrying 3 different missense mutations and several polymorphisms. Two different substitutions occurring in the same amino acidic position have been observed in 2 pati…

MaleAgingPopulationDNA Mutational AnalysisBiologyGene mutationmedicine.disease_causeGenetic analysisFUS geneMutant proteinALS; FUS gene; mutation; sporadicmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmyotrophic lateral sclerosiseducationAgedGeneticsAged 80 and overNeurologic ExaminationMutationeducation.field_of_studyGeneral NeuroscienceNeurodegenerationAmyotrophic Lateral SclerosisExonsMiddle AgedALS; FUS gene; Mutation; Sporadicmedicine.diseaseMagnetic Resonance ImagingSettore BIO/18 - GeneticasporadicMutationRNA-Binding Protein FUSFemaleSettore MED/26 - NeurologiaNeurology (clinical)ALSGeriatrics and GerontologyDevelopmental Biology
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C9ORF72 hexanucleotide repeat expansions in the Italian sporadic ALS population.

2012

It has been recently reported that a large proportion of patients with familial amyotrophic lateral sclerosis (familial ALS) and frontotemporal dementia (FTD) are associated with a hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72. We have assessed 1,757 Italian sporadic ALS cases, 133 from Sardinia, 101 from Sicily, and 1,523 from mainland Italy. Sixty (3.7%) of 1,624 mainland Italians and Sicilians and 9 (6.8%) of the 133 Sardinian sporadic ALS cases carried the pathogenic repeat expansion. None of the 619 regionally-matched control samples (1,238 chromosomes) carried the expansion. Twenty-five cases (36.2%) had behavioral FTD in addition to ALS. FTD or unspecified d…

MaleAgingSurvivalPedigree chartSettore MED/03 - GENETICA MEDICARepetitive Sequences0302 clinical medicineC9orf72Polymorphism (computer science)Risk FactorsPrevalenceAmyotrophic lateral sclerosisGenetics0303 health scienceseducation.field_of_studyGeneral NeuroscienceSingle NucleotideMiddle Aged3. Good healthSettore MED/26 - NEUROLOGIAItalyFemaleSettore MED/26 - NeurologiaFrontotemporal dementiaFrontotemporal dementiaGenetic MarkersPopulationC9ORF72BiologyPolymorphism Single NucleotideArticle03 medical and health sciencesmedicineHumansGenetic Predisposition to DiseasePolymorphismeducationamyotrophic lateral sclerosis; C9orf672; frontotemporal dementia; survivalAmyotrophic lateral sclerosi030304 developmental biologyRepetitive Sequences Nucleic AcidAmyotrophic lateral sclerosis; C9ORF72; sporadicC9orf72 ProteinNucleic AcidAmyotrophic lateral sclerosis C9ORF72 Frontotemporal dementia SurvivalGenetic VariationProteinsmedicine.diseaseAmyotrophic lateral sclerosisC9orf672C9orf72 ProteinAmyotrophic lateral sclerosis; C9ORF72; Frontotemporal dementia; Survival;Settore BIO/18 - GeneticasporadicNeurology (clinical)Geriatrics and GerontologyALSTrinucleotide repeat expansion030217 neurology & neurosurgeryDevelopmental Biology
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HFE p.H63D polymorphism does not influence ALS phenotype and survival.

2015

It has been recently reported that the p.His63Asp polymorphism of the HFE gene accelerates disease progression both in the SOD1 transgenic mouse and in amyotrophic lateral sclerosis (ALS) patients. We have evaluated the effect of HFE p.His63Asp polymorphism on the phenotype in 1351 Italian ALS patients (232 of Sardinian ancestry). Patients were genotyped for the HFE p.His63Asp polymorphism (CC, GC, and GG). All patients were also assessed for C9ORF72, TARDBP, SOD1, and FUS mutations. Of the 1351 ALS patients, 363 (29.2%) were heterozygous (GC) for the p.His63Asp polymorphism and 30 (2.2%) were homozygous for the minor allele (GG). Patients with CC, GC, and GG polymorphisms did not significa…

MaleAgingSurvivalSettore MED/03 - GENETICA MEDICAMiceSuperoxide Dismutase-1C9orf72HFE polymorphismAmyotrophic lateral sclerosisAmyotrophic lateral sclerosis; HFE polymorphisms; Phenotype; SOD1; Survival; Aged; Alleles; Amyotrophic Lateral Sclerosis; Animals; Disease Progression; Female; Hemochromatosis Protein; Histocompatibility Antigens Class I; Humans; Italy; Male; Membrane Proteins; Mice; Middle Aged; Polymorphism Genetic; Superoxide Dismutase; Superoxide Dismutase-1; Survival Rate; Genetic Association Studies; PhenotypeHFE polymorphismsMembrane ProteinAlleleAmyotrophic lateral sclerosis; HFE polymorphisms; Phenotype; SOD1; Survival; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyGeneral NeuroscienceSOD1Middle AgedPhenotypeSurvival RatePhenotypeItalyAmyotrophic lateral sclerosis; HFE polymorphisms; SOD1; phenotype; survivalDisease ProgressionFemaleHumanmedicine.medical_specialtySOD1Amyotrophic lateral sclerosis; HFE polymorphisms; Phenotype; SOD1; Survival;Genetic Association StudieBiologyTARDBPArticleGeneticInternal medicinemedicineAnimalsHumansAllelePolymorphismHemochromatosis ProteinSurvival rateAmyotrophic lateral sclerosiAllelesGenetic Association StudiesAgedNeuroscience (all)Polymorphism GeneticAnimalSuperoxide DismutaseAmyotrophic Lateral SclerosisHistocompatibility Antigens Class Inutritional and metabolic diseasesMembrane Proteinsmedicine.diseaseMinor allele frequencyEndocrinologyImmunologyNeurology (clinical)Geriatrics and GerontologyDevelopmental BiologyNeurobiology of aging
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