Search results for "Presenilin-1"

showing 10 items of 20 documents

Elevated Testosterone Level and Urine Scent Marking in Male 5xFAD Alzheimer Model Mice

2019

Background:Function of the Amyloid Precursor Protein (AβPP) and its various cleavage products still is not unraveled down to the last detail. While its role as a source of the neurotoxic Amyloid beta (Aβ) peptides in Alzheimer’s Disease (AD) is undisputed and its property as a cell attachment protein is intriguing, while functions outside the neuronal context are scarcely investigated. This is particularly noteworthy because AβPP has a ubiquitous expression profile and its longer isoforms, AβPP750 and 770, are found in various tissues outside the brain and in non-neuronal cells.Objective:Here, we aimed at analyzing the 5xFAD Alzheimer’s disease mouse model in regard to male sexual function.…

Male0301 basic medicinemedicine.medical_specialtymiceAmyloid betaCentral nervous system610Mice Transgenicamyloid precursor proteinAmyloid beta-Protein PrecursorSexual Behavior Animal03 medical and health sciences0302 clinical medicinesexual behaviorAlzheimer DiseaseInternal medicineTestisPresenilin-1medicineAmyloid precursor proteinAnimalsSperm CountbiologyWild typeBrainOrgan SizeAlzheimer's diseaseSertoli cellSpermPhenotypeAndrogen receptorDisease Models Animal030104 developmental biologymedicine.anatomical_structureEndocrinologyNeurologytestosteronebiology.proteinNeurology (clinical)030217 neurology & neurosurgeryurine scent marking test
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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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Circadian System Functionality, Hippocampal Oxidative Stress, and Spatial Memory in the APPswe/PS1dE9 Transgenic Model of Alzheimer Disease: Effects …

2012

Alzheimer disease (AD) is a neurodegenerative disorder that primarily causes β-amyloid accumulation in the brain, resulting in cognitive and behavioral deficits. AD patients, however, also suffer from severe circadian rhythm disruptions, and the underlying causes are still not fully known. Patients with AD show reduced systemic melatonin levels. This may contribute to their symptoms, since melatonin is an effective chronobiotic and antioxidant with neuroprotective properties. Here, the authors critically assessed the effects of long-term melatonin treatment on circadian system function, hippocampal oxidative stress, and spatial memory performance in the APPswe/PS1 double transgenic (Tg) mou…

Malemedicine.medical_specialtyPhysiologyChronobioticRamelteonReceptors MelatoninHippocampusMice TransgenicMotor Activitymedicine.disease_causeHippocampusNeuroprotectionBody TemperatureMelatoninAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseMemoryPhysiology (medical)Internal medicinePresenilin-1medicineAnimalsCircadian rhythmMelatoninmedicine.diseaseCircadian RhythmDisease Models AnimalOxidative StressEndocrinologyIndenesMutant ProteinsAlzheimer's diseasePsychologyNeuroscienceOxidative stressmedicine.drugChronobiology International
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Measurement of cerebral ABCC1 transport activity in wild-type and APP/PS1-21 mice with positron emission tomography

2020

Previous data suggest a possible link between multidrug resistance-associated protein 1 (ABCC1) and brain clearance of beta-amyloid (Aβ). We used PET with 6-bromo-7-[11C]methylpurine ([11C]BMP) to measure cerebral ABCC1 transport activity in a beta-amyloidosis mouse model (APP/PS1-21) and in wild-type mice aged 50 and 170 days, without and with pretreatment with the ABCC1 inhibitor MK571. One hundred seventy days-old-animals additionally underwent [11C]PiB PET scans to measure Aβ load. While baseline [11C]BMP PET scans detected no differences in the elimination slope of radioactivity washout from the brain (kelim) between APP/PS1-21 and wild-type mice of both age groups, PET scans after MK…

Mice TransgenicNeuroimaging03 medical and health sciencesAmyloid beta-Protein PrecursorMice0302 clinical medicineMethylpurineAlzheimer Diseasemental disordersmedicinePresenilin-1Animals030304 developmental biology0303 health sciencesmedicine.diagnostic_testbiologyTransport activityChemistryWild typeOriginal ArticlesMolecular biologyMice Inbred C57BLDisease Models AnimalNeurologyPositron emission tomographyPositron-Emission TomographyABCC1biology.proteinFemaleNeurology (clinical)Multidrug Resistance-Associated Protein 1Multidrug Resistance-Associated ProteinsRadiopharmaceuticalsCardiology and Cardiovascular Medicine030217 neurology & neurosurgeryJournal of Cerebral Blood Flow & Metabolism
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Effects of sulindac sulfide on the membrane architecture and the activity of gamma-secretase.

2007

gamma-Secretase is a membrane-embedded multi-protein complex that catalyzes the final cut of the Alzheimer's disease-related amyloid precursor protein (APP) to amyloid-beta peptides of variable length (37-43 amino acids) via an unusual intramembrane cleavage. Recent findings propose that some commonly used non-steroidal anti-inflammatory drugs (NSAIDs) have the ability to modulate specifically gamma-secretase activity without inhibiting the enzyme as a whole. These drugs may shift the processing of APP from the longer amyloid-beta 42 peptide towards shorter, less fibrillogenic and less toxic amyloid-beta species. We hypothesize that gamma-secretase activity, as an enzyme that is strictly as…

Protein subunitBlotting WesternPeptideCHO CellsSarcoplasmic Reticulum Calcium-Transporting ATPasesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorCricetulusMembrane MicrodomainsSulindacCricetinaemental disordersAmyloid precursor proteinPresenilin-1AnimalsHumansLipid raftCells CulturedPharmacologychemistry.chemical_classificationbiologyAnti-Inflammatory Agents Non-SteroidalCell MembraneP3 peptideAmino acidMembraneBiochemistrychemistrybiology.proteinBiophysicsAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseNeuropharmacology
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The natural history of Alzheimer disease: a longitudinal presymptomatic and symptomatic study of a familial cohort

2004

BACKGROUND: Knowledge of the evolution of cognitive deficits in Alzheimer disease is important for our understanding of disease progression. Previous reports, however, have either lacked detail or have not covered the presymptomatic stages. OBJECTIVE: To delineate the onset and progression of clinical and neuropsychological abnormalities in familial Alzheimer disease. METHODS: Nineteen subjects with familial Alzheimer disease underwent serial clinical and neuropsychological assessments. Eight of these had undergone presymptomatic assessments. The follow-up period was 1 to 10 years (mean, 5 years). The relative timing of the occurrence of 3 markers of disease onset and progression (onset of …

RISKSettore M-PSI/02 - Psicobiologia E Psicologia FisiologicaCOGNITIVE DECLINEPRESENILIN-1 MUTATIONDIAGNOSIS
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A novel mutation (Thr116IIe) in the presenilin 1 gene in a patient with early-onset Alzheimer's disease

2004

We report a novel presenilin 1 (PSN1) mutation (Thr116Ile) in a woman with early onset Alzheimer's disease (AD). This mutation was not found in 100 healthy controls, indicating that this is not a common polymorphism. The patient presented with forgetfulness at age 45, followed over the next 3 years by a worsening of the memory loss and frequent episodes of confusion and spatial disorientation. Neuroimaging studies were consistent with AD. The analysis of the family's pedigree showed that the proband was apparently the only member affected. Because the early death of several close relatives (i.e. the mother and the grandmother) and the demonstration that the father is not a mutation carrier,…

ThreonineProbandDNA Mutational AnalysisDiseaseBioinformaticsGenetic analysisPresenilinMutation CarrierAlzheimer DiseasePolymorphism (computer science)Presenilin-1medicineHumansEarly-onset Alzheimer's diseaseIsoleucineGeneticsbusiness.industryMembrane ProteinsMiddle Agedmedicine.diseaseNeurologyMutationMutation (genetic algorithm)FemaleSettore MED/26 - NeurologiaNeurology (clinical)businessAlzheimer's Disease Novel mutation Presenilin 1
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Insensitivity to Aβ42-lowering Nonsteroidal Anti-inflammatory Drugs and γ-Secretase Inhibitors Is Common among Aggressive Presenilin-1 Mutations

2007

Abeta42-lowering nonsteroidal anti-inflammatory drugs (NSAIDs) constitute the founding members of a new class of gamma-secretase modulators that avoid side effects of pan-gamma-secretase inhibitors on NOTCH processing and function, holding promise as potential disease-modifying agents for Alzheimer disease (AD). These modulators are active in cell-free gamma-secretase assays indicating that they directly target the gamma-secretase complex. Additional support for this hypothesis was provided by the observation that certain mutations in presenilin-1 (PS1) associated with early-onset familial AD (FAD) change the cellular drug response to Abeta42-lowering NSAIDs. Of particular interest is the P…

TransgeneMolecular Sequence DataMutantMice TransgenicCHO CellsBiologyPharmacologymedicine.disease_causeBiochemistryPresenilinMiceExonCricetulusAlzheimer DiseaseIn vivoCricetinaePresenilin-1medicineAnimalsHumansAmino Acid SequenceEnzyme InhibitorsMolecular BiologyMutationAmyloid beta-PeptidesSequence Homology Amino AcidDrug discoveryAnti-Inflammatory Agents Non-SteroidalCell BiologyPeptide FragmentsMutationbiology.proteinAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseJournal of Biological Chemistry
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Physical exercise neuroprotects ovariectomized 3xTg-AD mice through BDNF mechanisms.

2014

Postmenopausal women may be more vulnerable to cognitive loss and Alzheimer's disease (AD) than premenopausal women because of their deficiency in estrogens, in addition to their usually older age. Aerobic physical exercise has been proposed as a therapeutic approach for maintaining health and well-being in postmenopausal women, and for improving brain health and plasticity in populations at high risk for AD. To study the neuroprotective mechanisms of physical exercise in a postmenopausal animal model, we submitted previously ovariectomized, six-month old non-transgenic and 3xTg-AD mice to three months of voluntary exercise in a running wheel. At nine months of age, we observed lower grip s…

medicine.medical_specialtyBehavioral testsEndocrinology Diabetes and MetabolismOvariectomyP-CREBPhysical exerciseMice Transgenictau ProteinsCREBNeuroprotectionGrip strengthAmyloid beta-Protein PrecursorMiceEndocrinologyCognitionAlzheimer DiseaseInternal medicinePhysical Conditioning AnimalNeuroplasticitymedicinePresenilin-1DementiaAnimalsApathy3xTg-AD miceBiological PsychiatryNeuronsFrailtybiologyEndocrine and Autonomic SystemsBrain-Derived Neurotrophic FactorPhysical exerciseAlzheimer's diseaseCatalasemedicine.diseaseMice Inbred C57BLPsychiatry and Mental healthDisease Models AnimalBDNFEndocrinologyNeuroprotective AgentsCytoprotectionbiology.proteinOvariectomized ratFemalemedicine.symptomPsychologySignal TransductionPsychoneuroendocrinology
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Restoration of cerebral and systemic microvascular architecture in APP/PS1 transgenic mice following treatment with Liraglutide™.

2015

OBJECTIVE: Cerebral microvascular impairments occurring in AD may reduce Aβ peptide clearance and impact upon circulatory ultrastructure and function. We hypothesized that microvascular pathologies occur in organs responsible for systemic Aβ peptide clearance in a model of AD and that Liraglutide (Victoza(®)) improves vessel architecture. METHODS: Seven-month-old APP/PS1 and age-matched wild-type mice received once-daily intraperitoneal injections of either Liraglutide or saline (n = 4 per group) for eight weeks. Casts of cerebral, splenic, hepatic, and renal microanatomy were analyzed using SEM. RESULTS: Casts from wild-type mice showed regularly spaced microvasculature with smooth lumenal…

medicine.medical_specialtyPhysiologySpleenMice TransgenicKidneyMicrocirculationAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseGlucagon-Like Peptide 1Physiology (medical)Internal medicinemedicinePresenilin-1AnimalsHumansHypoglycemic AgentsMolecular BiologyKidneybusiness.industryLiraglutideMicrocirculationBrainLiraglutideGlucagon-like peptide-1Extravasationmedicine.anatomical_structureEndocrinologyCerebrovascular CirculationCirculatory systemMicrovesselsSystemic administrationCardiology and Cardiovascular MedicinebusinessSpleenmedicine.drugMicrocirculation (New York, N.Y. : 1994)
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