Search results for "Apolipoprotein"

showing 10 items of 354 documents

Relationship Between Body Mass Index, ApoE4 Status, and PET-Based Amyloid and Neurodegeneration Markers in Amyloid-Positive Subjects with Normal Cogn…

2018

Body weight loss in late-life is known to occur at a very early stage of Alzheimer's disease (AD). Apolipoprotein E4 (ApoE4) represents a major genetic risk factor for AD and is linked to an increased cortical amyloid-β (Aβ) accumulation. Since the relationship between body weight, ApoE4, and AD pathology is poorly investigated, we aimed to evaluate whether ApoE4 allelic status modifies the association of body mass index (BMI) with markers of AD pathology. A total of 368 Aβ-positive cognitively healthy or mild cognitive impaired subjects had undergone [18F]-AV45-PET, [18F]-FDG-PET, and T1w-MRI examinations. Composite cortical [18F]-AV45 uptake and [18F]-FDG uptake in posterior cingulate cor…

0301 basic medicineMaleApolipoprotein E4Body Mass Index0302 clinical medicineCognitionWeight lossCognitive declineAniline CompoundsGeneral NeuroscienceNeurodegenerationBrainCognitionNeurodegenerative DiseasesGeneral MedicinePsychiatry and Mental healthClinical PsychologyEthylene GlycolsFemalemedicine.symptommedicine.medical_specialtyAmyloidHeterozygote03 medical and health sciencesFluorodeoxyglucose F18Internal medicinemental disordersWeight LossmedicineHumansCognitive DysfunctionEffects of sleep deprivation on cognitive performanceAdaptor Proteins Signal TransducingAgedbusiness.industryZebrafish Proteinsmedicine.diseaseCortex (botany)Repressor Proteins030104 developmental biologyEndocrinologyGlucosePosterior cingulatePositron-Emission TomographyGeriatrics and GerontologyRadiopharmaceuticalsbusinessNeuroscienceBody mass index030217 neurology & neurosurgeryFollow-Up StudiesJournal of Alzheimer's disease : JAD
researchProduct

Rare Pathogenic Variants Predispose to Hepatocellular Carcinoma in Nonalcoholic Fatty Liver Disease

2019

AbstractNonalcoholic fatty liver disease (NAFLD) is a rising cause of hepatocellular carcinoma (HCC). We examined whether inherited pathogenic variants in candidate genes (n = 181) were enriched in patients with NAFLD-HCC. To this end, we resequenced peripheral blood DNA of 142 NAFLD-HCC, 59 NAFLD with advanced fibrosis, and 50 controls, and considered 404 healthy individuals from 1000 G. Pathogenic variants were defined according to ClinVar, likely pathogenic as rare variants predicted to alter protein activity. In NAFLD-HCC patients, we detected an enrichment in pathogenic (p = 0.024), and likely pathogenic variants (p = 1.9*10−6), particularly in APOB (p = 0.047). APOB variants were asso…

0301 basic medicineMaleCandidate geneApolipoprotein Blcsh:MedicineGastroenterologyLiver diseasechemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseSequestosome-1 ProteinGenetic riskHCClcsh:ScienceMultidisciplinarybiologyLiver NeoplasmsMiddle Aged3. Good healthCholesterolHepatocellular carcinomaApolipoprotein B-100FemaleAged; Apolipoprotein B-100; Carcinoma Hepatocellular; Case-Control Studies; Cholesterol HDL; Female; Genetic Predisposition to Disease; Glial Cell Line-Derived Neurotrophic Factor Receptors; Humans; Liver Neoplasms; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Reproducibility of Results; Risk Factors; Sequestosome-1 Proteinmedicine.medical_specialtyCarcinoma HepatocellularGlial Cell Line-Derived Neurotrophic Factor ReceptorsHDLSettore BIO/18 - GENETICAdigestive systemArticle03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseGeneAgedCholesterolbusiness.industrylcsh:RCarcinomaCholesterol HDLnutritional and metabolic diseasesReproducibility of ResultsHepatocellularmedicine.diseasedigestive system diseases030104 developmental biologychemistryNASH HCCCase-Control Studiesbiology.proteinlcsh:Qgeneticbusiness030217 neurology & neurosurgery
researchProduct

Alzheimer's disease in the gut : major changes in the gut of 5xFAD model mice with ApoA1 as potential key player

2019

Alzheimer's disease (AD) affects around 33 million people worldwide, which makes it the most prominent form of dementia. The main focus of AD research has been on the central nervous system (CNS) for long, but in recent years, the gut gained more attention. The intestinal tract is innervated by the enteric nervous system (ENS), built of numerous different types of neurons showing great similarity to neurons of the CNS. It already has been demonstrated that the amyloid precursor protein, which plays a major role in AD pathology, is also expressed in these cells. We analyzed gut tissue of AD model mice (5xFAD) and the respective wild-type littermates at different pathological stages: pre-path…

0301 basic medicineMaleColonCentral nervous system610 MedizinMice TransgenicDiseaseBiochemistryEnteric Nervous System03 medical and health sciencesMice0302 clinical medicineAlzheimer Disease610 Medical sciencesGeneticsmedicineAmyloid precursor proteinDementiaAnimalsViability assayMolecular BiologyPathologicalbiologyApolipoprotein A-Imedicine.diseaseDisease Models Animal030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinEnteric nervous systemFOXA2030217 neurology & neurosurgeryBiotechnology
researchProduct

Clinical and biochemical characteristics of individuals with low cholesterol syndromes: A comparison between familial hypobetalipoproteinemia and fam…

2017

Background The most frequent monogenic causes of low plasma cholesterol are familial hypobetalipoproteinemia (FHBL1) because of truncating mutations in apolipoprotein B coding gene (APOB) and familial combined hypolipidemia (FHBL2) due to loss-of-function mutations in ANGPTL3 gene. Objective A direct comparison of lipid phenotypes of these 2 conditions has never been carried out. In addition, although an increased prevalence of liver steatosis in FHBL1 has been consistently reported, the hepatic consequences of FHBL2 are not well established. Methods We investigated 350 subjects, 67 heterozygous carriers of APOB mutations, 63 carriers of the p.S17* mutation in ANGPTL3 (57 heterozygotes and …

0301 basic medicineMaleHepatic steatosisSettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematologymedicine.disease_causeANGPTL3 gene; APOB gene; Familial combined hypolipidemia; Familial hypobetalipoproteinemia; HDL cholesterol; Hepatic steatosis; Low cholesterol syndromesHypobetalipoproteinemiasExon0302 clinical medicineHDL cholesterolANGPTL3Nutrition and DieteticFamilial hypobetalipoproteinemiaGeneticsMutationNutrition and Dieteticsbiologyhepatic steatosisHomozygoteANGPTL3 geneMiddle AgedLow cholesterol syndromesPhenotypePhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineANGPTL3 gene; APOB gene; familial combined hypolipidemia; familial hypobetalipoproteinemia; HDL cholesterol; hepatic steatosis; low cholesterol syndromesmedicine.medical_specialtyHeterozygoteLow cholesterol syndromeHepatic steatosi03 medical and health sciencesInternal medicineInternal MedicinemedicineHumansAPOB geneFamilial combined hypolipidemiaGeneAgedAngiopoietin-Like Protein 3Apolipoproteins Bbusiness.industryHeterozygote advantagemedicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsMutationbiology.proteinlow cholesterol syndromesSteatosisbusiness
researchProduct

Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
researchProduct

Oxidative signature of cerebrospinal fluid from mild cognitive impairment and Alzheimer disease patients

2015

Abstract Background Several studies suggest that pathological changes in Alzheimer’s disease (AD) brain begin around 10–20 years before the onset of cognitive impairment. Biomarkers that can support early diagnosis and predict development of dementia would, therefore, be crucial for patient care and evaluation of drug efficacy. Although cerebrospinal fluid (CSF) levels of Aβ42, tau, and p-tau are well-established diagnostic biomarkers of AD, there is an urgent need to identify additional molecular alterations of neuronal function that can be evaluated at the systemic level. Objectives This study was focused on the analysis of oxidative stress-related modifications of the CSF proteome, from …

0301 basic medicineOncologyPathologyDiseasephysiology (medical)medicine.disease_causeProtein oxidationtau proteins0302 clinical medicineCerebrospinal fluidmiddle aged80 and overoxidative stresshumansAged 80 and overamyloid beta-peptidesredox proteomicsagedfemale030220 oncology & carcinogenesisBiomarker (medicine)Alzheimer's diseaseAlzheimer diseaseAPOEmedicine.medical_specialtyoxidation-reductionproteomeCSFmolecular sequence data03 medical and health sciencesmalecognitive dysfunctionInternal medicinemental disordersmedicineDementiabiochemistryprotein oxidationbusiness.industrypeptide fragmentscase-control studiesCase-control studybiomarkersmedicine.diseaseAPOE; biomarkers; CSF; extracellular chaperones; protein oxidation; redox proteomics; aged; aged 80 and over; Alzheimer disease; amino acid sequence; amyloid beta-peptides; apolipoproteins E; biomarkers; case-control studies; cognitive dysfunction; female; humans; male; middle aged; molecular sequence data; oxidation-reduction; oxidative stress; peptide fragments; proteome; tau proteins; biochemistry; physiology (medical)extracellular chaperonesamino acid sequence030104 developmental biologybusinessOxidative stressapolipoproteins E
researchProduct

Short telomere length is associated with impaired cognitive performance in European ancestry cohorts

2017

AbstractThe association between telomere length (TL) dynamics on cognitive performance over the life-course is not well understood. This study meta-analyses observational and causal associations between TL and six cognitive traits, with stratifications on APOE genotype, in a Mendelian Randomization (MR) framework. Twelve European cohorts (N=17 052; mean age=59.2±8.8 years) provided results for associations between qPCR-measured TL (T/S-ratio scale) and general cognitive function, mini-mental state exam (MMSE), processing speed by digit symbol substitution test (DSST), visuospatial functioning, memory and executive functioning (STROOP). In addition, a genetic risk score (GRS) for TL includin…

0301 basic medicineOncologycognitionNetherlands Twin Register (NTR)Psychometricsgenetic associationgenotypepolymerase chain reactionStatistics as TopicNeuropsychological Testsgenetic riskDISEASE3124 Neurology and psychiatryCohort Studies0302 clinical medicinesingle nucleotide polymorphismcognitive defectYOUNG-ADULTSgenetic variabilitytelomere lengthMedicineGWAScognitive performanceta515depth perceptionNetherlandsRISKlearningmedicine.diagnostic_testdigit symbol substitution testquantitative analysisDEMENTIAGenetic Carrier ScreeningadultarticleMini Mental State ExaminationCognitionta3142episodic memoryznf208 geneMiddle AgedTelomereapolipoprotein E4cohort analysisrtel1 genePsychiatry and Mental healthPROCESSING SPEEDacyp2 genefemaleancestry groupMENDELIAN RANDOMIZATIONOriginal ArticleClinical psychologymedicine.medical_specialtytert genePsychometricsMendelian randomization analysisgenetic risk scoreWhite People03 medical and health sciencesCellular and Molecular NeurosciencemaleInternal medicineMendelian randomizationpleiotropyJournal Article/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_HumansCognitive DysfunctionEffects of sleep deprivation on cognitive performancehumangeneBiological PsychiatryMETAANALYSISAgedterc geneStroop testMini–Mental State Examinationgenome-wide association studyIDENTIFICATIONPsykologi (exklusive tillämpad psykologi)business.industryMORTALITYobfc1 genemajor clinical studyConfidence intervalPsychology (excluding Applied Psychology)030104 developmental biologyexecutive functionDigit symbol substitution testnaf1 geneobservational studybusiness030217 neurology & neurosurgeryStroop effect
researchProduct

Association between familial hypobetalipoproteinemia and the risk of diabetes. Is this the other side of the cholesterol-diabetes connection? A syste…

2017

Statin therapy is beneficial in reducing LDL cholesterol (LDL-C) levels and cardiovascular events, but it is associated with the risk of incident diabetes mellitus (DM). Familial hypercholesterolemia (FH) is characterized by genetically determined high levels of plasma LDL-C and a low prevalence of DM. LDL-C levels seem then inversely correlated with prevalence of DM. Familial hypobetalipoproteinemia (FHBL) represents the genetic mirror of FH in terms of LDL-C levels, very low in subjects carrying mutations of APOB, PCSK9 (FHBL1) or ANGPTL3 (FHBL2). This review explores the hypothesis that FHBL might represent also the genetic mirror of FH in terms of prevalence of DM and that it is expecte…

0301 basic medicineProbandMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and MetabolismPopulationPrevalenceFamilial hypercholesterolemia030204 cardiovascular system & hematologyHypobetalipoproteinemias03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyInternal medicineDiabetes mellitusInternal MedicinemedicineDiabetes MellitusPrevalenceHumansFamilial hypobetalipoproteinemiaDiabetes mellitus riskeducationeducation.field_of_studybiologyCholesterolbusiness.industryPCSK9StatinsStatinGeneral MedicineCholesterol LDLFamilial hypobetalipoproteinemia; Cholesterol; Diabetes mellitus risk ;Statinsmedicine.diseaseFamilial hypobetalipoproteinemia-Cholesterol- Diabetes mellitus risk- Statins030104 developmental biologyEndocrinologyCholesterolchemistrybiology.proteinlipids (amino acids peptides and proteins)Femalebusiness
researchProduct

Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
researchProduct

The potential role of mitochondrial ATP synthase inhibitory factor 1 (IF1) in coronary heart disease: a literature review

2017

Cardiovascular disease (CVD) is the leading cause of death worldwide, and so the search for innovative and accurate biomarkers for guiding prevention, diagnosis, and treatment is a valuable clinical and economic endeavor. Due to a recent findings that the serum concentration of mitochondrial ATP synthase inhibitory factor 1 (IF1) is an independent prognostic factor in patients with coronary heart disease (CHD), we reviewed the role of this protein in myocardial ischemic preconditioning, its correlation to plasma high density lipoprotein (HDL), the predictive potential in patients with CHD, and its interplay with angiogenesis. IF1 has been positively correlated with plasma HDL-cholesterol, a…

0301 basic medicinemedicine.medical_specialtyClinical chemistryAngiogenesisEndocrinology Diabetes and MetabolismInhibitory factor 1Clinical BiochemistryHigh density lipoproteinCoronary DiseaseClinical nutritionDiseaseReview030204 cardiovascular system & hematologyBioinformaticsMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundAngiogenesis; Cardiovascular disease; High density lipoprotein; Inhibitory factor 10302 clinical medicineEndocrinologyHigh-density lipoproteinInternal medicineMedicineHumansCause of deathBiochemistry medicalbiologybusiness.industryBiochemistry (medical)ProteinsCardiovascular diseaseMitochondria030104 developmental biologyEndocrinologychemistrybiology.proteinIschemic preconditioningApolipoprotein A1AngiogenesisbusinessLipids in Health and Disease
researchProduct