Search results for "AMYLOID"

showing 10 items of 494 documents

Amyloidosis and Ocular Involvement: an Overview.

2019

Purpose: To describe the ophthalmic manifestations of amyloidosis and the corresponding therapeutic measures.Methods: The 178 patients included in the study had different types of amyloidosis, diagnosed at a single internal medicine institution (Bari, Italy). To provide a comprehensive review of the types of amyloidosis that can be associated with ocular involvement, the images and clinical descriptions of patients with amyloidosis structurally related to gelsolin, keratoepithelin and lactoferrin were obtained in collaborations with the ophthalmology departments of hospitals in Mainz (Germany) and Helsinki (Finland).Results: Overall, ocular morbidity was detected in 41 of the 178 patients w…

MalePathologymedicine.medical_specialtygenetic structuresEye Diseasesmedicine.medical_treatmentCorneal dystrophyDiagnostic Techniques OphthalmologicalEye03 medical and health sciences0302 clinical medicineAA amyloidosismedicineAL amyloidosisHumansCorneal transplantationCorneal epitheliumRetrospective Studiesbiologybusiness.industryAmyloidosisGeneral MedicineAmyloidosisMiddle Agedmedicine.diseaseeye diseases3. Good healthOphthalmologyTransthyretinmedicine.anatomical_structure030221 ophthalmology & optometrybiology.proteinLattice corneal dystrophyFemalesense organsbusiness030217 neurology & neurosurgeryFollow-Up StudiesSeminars in ophthalmology
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Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer's disease patients: A neuroimaging biomarker of the disease.

2017

Purpose The objective of this study was to correlate the presence and distribution of cerebral microbleeds in Alzheimer’s disease patients with cerebrospinal fluid biomarkers (amyloid-beta and phosphorylated tau 181 protein levels) and cognitive decline by using susceptibility-weighted imaging magnetic resonance sequences at 1.5 T. Material and methods Fifty-four consecutive Alzheimer’s disease patients underwent brain magnetic resonance imaging at 1.5 T to assess the presence and distribution of cerebral microbleeds on susceptibility-weighted imaging images. The images were analyzed in consensus by two neuroradiologists, each with at least 10 years’ experience. Dementia severity was assess…

MalePathologymedicine.medical_specialtytau ProteinsDisease030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineCerebrospinal fluidNeuroimagingAlzheimer DiseasemedicineHumansRadiology Nuclear Medicine and imagingAlzheimer's disease; Cerebral microbleeds; magnetic resonance imaging; susceptibility-weighted imaging; Radiology Nuclear Medicine and Imaging; Neurology (clinical)AgedCerebral HemorrhageAmyloid beta-Peptidesmedicine.diagnostic_testbusiness.industryCerebral microbleedBrainMagnetic resonance imagingGeneral MedicineAlzheimer's diseaseMagnetic Resonance Imagingsusceptibility-weighted imagingSusceptibility weighted imagingBiomarker (medicine)FemaleNeurology (clinical)business030217 neurology & neurosurgeryBiomarkersThe neuroradiology journal
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A second family with familial AD and the V717L APP mutation has a later age at onset

2006

Four mutations have been reported at the 717 codon of the amyloid precursor protein (APP), with valine substituted by isoleucine, glycine, phenylalanine, and leucine. While several families with the isoleucine substitution have been described, the other substitutions have been reported in only one family each worldwide. A family with the V717L APP mutation has been previously reported,1 with a mean age at onset of 38 years (range 35 to 39), based on four affected family members, and a mean age at death of 46 years (range 40 to 50). We have identified a second family with a later mean age at onset of 50 years (range 48 to 57) and mean age at death of 61 years (range 57 to 68). Family 171 is …

MalePediatricsmedicine.medical_specialtyMutation Missensemedicine.disease_causeAmyloid beta-Protein PrecursorAlzheimer DiseaseValineInternal medicinemedicineAmyloid precursor proteinHumansAge of OnsetAgedAge of Onset Aged Alzheimer Disease/genetics Alzheimer Disease/physiopathology Amino Acid Substitution Amyloid beta-Protein Precursor/genetics Female Humans Malle Middle Aged Mutation Missense PedigreeMutationSettore M-PSI/02 - Psicobiologia E Psicologia FisiologicabiologyMean ageMiddle AgedPedigreeEndocrinologyAmino Acid Substitutionbiology.proteinFemaleNeurology (clinical)IsoleucineNeurology
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Why Women Have More Alzheimer's Disease Than Men: Gender and Mitochondrial Toxicity of Amyloid-β Peptide

2010

The main risk factors for developing Alzheimer's disease (AD) are age and gender. The incidence of the disease is higher in women than in men, and this cannot simply be attributed to the higher longevity of women versus men. Thus, there must be a specific pathogenic mechanism to explain the higher incidence of AD cases in women. In this regard, it is notable that mitochondria from young females are protected against amyloid-beta toxicity, generate less reactive oxygen species, and release less apoptogenic signals than those from males. However, all this advantage is lost in mitochondria from old females. Since estrogenic compounds protect against mitochondrial toxicity of amyloid-beta, estr…

MalePhysiologyDiseaseMitochondrionPharmacologyModels BiologicalAlzheimer DiseaseRisk FactorsmedicineHumansSex CharacteristicsAmyloid beta-PeptidesbiologyGinkgo bilobaGeneral NeuroscienceIncidence (epidemiology)EstrogensGeneral Medicinebiology.organism_classificationmedicine.diseaseMitochondriaUp-RegulationClinical trialPsychiatry and Mental healthClinical PsychologyMitochondrial toxicityToxicityFemaleGeriatrics and GerontologySex characteristicsJournal of Alzheimer's Disease
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Oligodendrocyte precursor cells modulate the neuronal network by activity-dependent ectodomain cleavage of glial NG2.

2014

The role of glia in modulating neuronal network activity is an important question. Oligodendrocyte precursor cells (OPC) characteristically express the transmembrane proteoglycan nerve-glia antigen 2 (NG2) and are unique glial cells receiving synaptic input from neurons. The development of NG2+ OPC into myelinating oligodendrocytes has been well studied, yet the retention of a large population of synapse-bearing OPC in the adult brain poses the question as to additional functional roles of OPC in the neuronal network. Here we report that activity-dependent processing of NG2 by OPC-expressed secretases functionally regulates the neuronal network. NG2 cleavage by the α-secretase ADAM10 yields…

MaleQH301-705.5ADAM10Long-Term PotentiationAMPA receptorReceptors N-Methyl-D-AspartateGeneral Biochemistry Genetics and Molecular BiologyCell LineADAM10 ProteinMiceBiological neural networkAnimalsBiology (General)AntigensMice KnockoutNeuronsNeuronal PlasticityGeneral Immunology and MicrobiologybiologyGeneral NeurosciencePyramidal CellsGlutamate receptorMembrane ProteinsBiology and Life SciencesLong-term potentiationSensory GatingCell biologyExtracellular MatrixProtein Structure Tertiarystomatognathic diseasesADAM ProteinsOligodendrogliaBiochemistryEctodomainnervous systemReceptors GlutamateSynapsesbiology.proteinSynopsisNMDA receptorProteoglycansAmyloid Precursor Protein SecretasesGeneral Agricultural and Biological SciencesAmyloid precursor protein secretaseNeurosciencePLoS biology
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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Monitoring effectiveness and safety of Tafamidis in transthyretin amyloidosis in Italy: a longitudinal multicenter study in a non-endemic area

2016

Tafamidis is a transthyretin (TTR) stabilizer able to prevent TTR tetramer dissociation. There have been a few encouraging studies on Tafamidis efficacy in early-onset inherited transthyretin amyloidosis (ATTR) due to Val30Met mutation. However, less is known about its efficacy in later disease stages and in non-Val30Met mutations. We performed a multi-center observational study on symptomatic ATTR patients prescribed to receive Tafamidis. We followed up patients according to a standardized protocol including general medical, cardiological and neurological assessments at baseline and every 6 months up to 3 years. Sixty-one (42 males) patients were recruited. Only 28 % of enrolled subjects h…

MaleTafamidisAmyloid polyneuropathyNeurologyCardiomyopathyDisease030204 cardiovascular system & hematologySeverity of Illness IndexTransthyretinchemistry.chemical_compound0302 clinical medicinePrealbuminTafamidiLongitudinal StudiesStage (cooking)Aged 80 and overBenzoxazolesbiologyAmyloidosisMiddle Agedamyloid polyneuropathy; tafamidis; transthyretinPrognosisTafamidisSettore MED/26 - NEUROLOGIATreatment OutcomeItalyNeurologyDisease ProgressionFemaleAmyloid polyneuropathy; Tafamidis; Transthyretin; Neurology (clinical); NeurologyAdultmedicine.medical_specialty03 medical and health sciencesInternal medicineSeverity of illnessmedicineHumansAgedAmyloid Neuropathies Familialbusiness.industrynutritional and metabolic diseasesmedicine.diseaseSurgeryTransthyretinchemistryMutationbiology.proteinNeurology (clinical)business030217 neurology & neurosurgeryFollow-Up StudiesJournal of Neurology
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Association between IgM Anti-Herpes Simplex Virus and Plasma Amyloid-Beta Levels.

2011

International audience; OBJECTIVE: Herpes simplex virus (HSV) reactivation has been identified as a possible risk factor for Alzheimer's disease (AD) and plasma amyloid-beta (Aβ) levels might be considered as possible biomarkers of the risk of AD. The aim of our study was to investigate the association between anti-HSV antibodies and plasma Aβ levels. METHODS: The study sample consisted of 1222 subjects (73.9 y in mean) from the Three-City cohort. IgM and IgG anti-HSV antibodies were quantified using an ELISA kit, and plasma levels of Aβ(1-40) and Aβ(1-42) were measured using an xMAP-based assay technology. Cross-sectional analyses of the associations between anti-HSV antibodies and plasma …

MaleViral DiseasesApolipoprotein BEpidemiology[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionmedicine.disease_causePathogenesis0302 clinical medicineBlood plasmaPathology[ SHS.INFO ] Humanities and Social Sciences/Library and information sciencesSimplexvirusNeuropathology0303 health sciencesMultidisciplinarybiologyQRObstetrics and Gynecology3. Good healthInfectious DiseasesNeurologyMedicineFemaleAlzheimer's diseaseAntibodyResearch ArticleAmyloid betaUrologyScience[SHS.INFO]Humanities and Social Sciences/Library and information sciencesSexually Transmitted DiseasesEnzyme-Linked Immunosorbent Assay[SHS.INFO] Humanities and Social Sciences/Library and information sciences03 medical and health sciencesDiagnostic MedicineAlzheimer DiseasemedicineHumansAged030304 developmental biologyAmyloid beta-PeptidesGenitourinary InfectionsHerpes Simplexmedicine.diseasePeptide FragmentsHerpes Simplex Virus[SDV.AEN] Life Sciences [q-bio]/Food and NutritionHerpes simplex virusImmunoglobulin MAnatomical PathologyImmunoglobulin MImmunologybiology.proteinDementiaVirus Activation[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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Metformin increases APP expression and processing via oxidative stress, mitochondrial dysfunction and NF-κB activation: Use of insulin to attenuate m…

2015

AbstractClinical and experimental biomedical studies have shown Type 2 diabetes mellitus (T2DM) to be a risk factor for the development of Alzheimer's disease (AD). This study demonstrates the effect of metformin, a therapeutic biguanide administered for T2DM therapy, on β-amyloid precursor protein (APP) metabolism in in vitro, ex vivo and in vivo models. Furthermore, the protective role of insulin against metformin is also demonstrated. In LAN5 neuroblastoma cells, metformin increases APP and presenilin levels, proteins involved in AD. Overexpression of APP and presenilin 1 (Pres 1) increases APP cleavage and intracellular accumulation of β-amyloid peptide (Aβ), which, in turn, promotes ag…

Maleendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causeAntioxidantsNF-κBAmyloid beta-Protein PrecursorAspartic Acid EndopeptidasesInsulinBiguanideNF-kappa BBrainAlzheimer's diseaseMetforminMetforminMitochondriaProtein TransportAntioxidantmedicine.drugmetformin T2DM Alzheimer's diseaseAdultmedicine.medical_specialtyProgrammed cell deathmedicine.drug_classOxidative phosphorylationBiologyAntidiabetic drugModels BiologicalPresenilinInternal medicineCell Line Tumormental disordersmedicinePresenilin-1AnimalsHumansMolecular BiologyCell NucleusSettore MED/04 - Patologia GeneraleAmyloid beta-PeptidesInsulinAdenylate KinaseOxidative Stress Pathwaynutritional and metabolic diseasesCell BiologyHydrogen PeroxideMice Inbred C57BLEndocrinologyGene Expression RegulationCytoprotectionOxidative stressLeukocytes MononuclearAmyloid Precursor Protein SecretasesOxidative stressBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Familial Mediterranean Fever: an unusual cause of liver disease

2019

Abstract Background Familial Mediterranean Fever is an autoinflammatory disease typically expressed with recurrent attacks of fever, serositis, aphthous stomatitis, rash. Only a few reports describe the association with hepatic involvement. Case presentation We describe the clinical case of a child affected, since the age of 1 year, by recurrent fever, aphthous stomatitis, rash, arthralgia, associated with abdominal pain, vomiting, lymphadenopathy. The diagnosis of Familial Mediterranean Fever was confirmed by the genetic study of MEFV gene; the homozygous mutation M694 V in exon was documented. A partial control of attacks was obtained with colchicine. The child continued to manifest only …

Malemedicine.medical_specialtyAbdominal painCanakinumabFamilial Mediterranean feverCase ReportFamilial Mediterranean feverGastroenterology03 medical and health scienceschemistry.chemical_compoundLiver disease0302 clinical medicineSettore MED/38 - Pediatria Generale E Specialistica030225 pediatricsInternal medicineHumansMedicineColchicine030212 general & internal medicineSerum amyloid AChildbusiness.industryLiver Diseaseslcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseMEFVRashchemistrymedicine.symptombusinessColchicineSerositisLiver diseaseItalian Journal of Pediatrics
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