Search results for "Presenilin-1"

showing 10 items of 20 documents

Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer's Disease-Like Pathophysiology in APP/PS1 Mice.

2019

Glutamate excitotoxicity has long been related to Alzheimer's disease (AD) pathophysiology, and it has been shown to affect the major AD-related hallmarks, amyloid-β peptide (Aβ) accumulation and tau phosphorylation (p-tau). We investigated whether oral administration of monosodium glutamate (MSG) has effects in a murine model of AD, the double transgenic mice APP/PS1. We found that AD pathogenic factors appear earlier in APP/PS1 when supplemented with MSG, while wildtype mice were essentially not affected. Aβ and p-tau levels were increased in the hippocampus in young APP/PS1 animals upon MSG administration. This was correlated with increased Cdk5-p25 levels. Furthermore, in these mice, we…

0301 basic medicineGenetically modified mouseMalemedicine.medical_specialtyMonosodium glutamateExcitotoxicityHippocampusAdministration OralMice TransgenicAMPA receptormedicine.disease_cause03 medical and health scienceschemistry.chemical_compoundAmyloid beta-Protein PrecursorMice0302 clinical medicineOral administrationAlzheimer DiseaseInternal medicinemental disordersSodium GlutamatemedicinePresenilin-1Animalsbusiness.industryGeneral NeuroscienceGlutamate receptorLong-term potentiationGeneral MedicineFlavoring AgentsPsychiatry and Mental healthClinical Psychology030104 developmental biologyEndocrinologychemistryFemaleGeriatrics and Gerontologybusiness030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Short-Term Effects of Microglia-Specific Mitochondrial Dysfunction on Amyloidosis in Transgenic Models of Alzheimer's Disease.

2018

Reduction of mitochondrial activity is a subtle and early event in the pathogenesis of Alzheimer’s disease. Mitochondrial damage and consequentially enhanced production of reactive oxygen species is particularly occurring in the vicinity of amyloid plaques. Since all cells are affected by mitochondrial damage, analyses of cell type-specific effects are challenging. To study the impact of mitochondrial alterations on microglial activity in a homogeneous genetic background, we generated bone marrow chimeras of irradiated 46-days-old APP-transgenic mice. For reconstitution, bone marrow from CX3CR1-eGFP mice with mitochondria of either non-obese diabetic or C57BL/6J animals was utilized. Succes…

0301 basic medicineMalePathologymedicine.medical_specialtyMitochondrial DiseasesAmyloidCellGreen Fluorescent ProteinsCX3C Chemokine Receptor 1Mice TransgenicPlaque AmyloidBiologyMitochondrionPathogenesis03 medical and health sciencesAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseMice Inbred NODCX3CR1medicinePresenilin-1AnimalsHumansMicrogliaGeneral NeuroscienceAmyloidosisCalcium-Binding ProteinsMicrofilament ProteinsGeneral MedicineAmyloidosismedicine.diseaseMitochondriaMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureFemaleBone marrowMicrogliaGeriatrics and Gerontology030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Altered Gut Microbiome Composition and Tryptic Activity of the 5xFAD Alzheimer's Mouse Model.

2017

The regulation of physiological gut functions such as peristalsis or secretion of digestive enzymes by the central nervous system via the Nervus vagus is well known. Recent investigations highlight that pathological conditions of neurological or psychiatric disorders might directly interfere with the autonomous neuronal network of the gut - the enteric nervous system, or even derive from there. By using a murine Alzheimer's disease model, we investigated a potential influence of disease-associated changes on gastrointestinal properties. 5xFAD mice at three different ages were compared to wild type littermates in regard to metabolic parameters and enzymes of the gut by fluorimetric enzyme as…

0301 basic medicineMalemedicine.medical_specialtyAgingColonTransgeneCentral nervous systemMice TransgenicBiologyPresenilin03 medical and health sciencesAmyloid beta-Protein PrecursorEatingFeces0302 clinical medicineAlzheimer DiseaseInternal medicinemedicinePresenilin-1AnimalsHumansTrypsinMicrobiomeGeneral NeuroscienceGastrointestinal MicrobiomeBody WeightWild typeGeneral Medicinemedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureEndocrinologyImmunologyEnteric nervous systemGeriatrics and GerontologyAlzheimer's disease030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Down-regulation of Endogenous Amyloid Precursor Protein Processing due to Cellular Aging

2005

Processing of amyloid precursor protein (APP) is a well acknowledged central pathogenic mechanism in Alzheimer disease. However, influences of age-associated cellular alterations on the biochemistry of APP processing have not been studied in molecular detail so far. Here, we report that processing of endogenous APP is down-regulated during the aging of normal human fibroblasts (IMR-90). The generation of intracellular APP cleavage products C99, C83, and AICD gradually declines with increasing life span and is accompanied by a reduced secretion of soluble APP (sAPP) and sAPPalpha. Further, the maturation of APP was reduced in senescent cells, which has been shown to be directly mediated by a…

ADAM10NicastrinEndogenyBiochemistryCell LineAmyloid beta-Protein PrecursorMembrane MicrodomainsDownregulation and upregulationEndopeptidasesmental disordersPresenilin-1Amyloid precursor proteinAspartic Acid EndopeptidasesHumansSecretionMolecular BiologyCellular SenescenceMembrane GlycoproteinsbiologyChemistryMembrane ProteinsCell BiologyFibroblastsCholesterolBiochemistrybiology.proteinAmyloid Precursor Protein SecretasesProtein Processing Post-TranslationalAmyloid precursor protein secretaseIntracellularJournal of Biological Chemistry
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Altered morphological and electrophysiological properties of Cajal-Retzius cells in cerebral cortex of embryonic Presenilin-1 knockout mice

2004

Mutations of Presenilin-1 are the major cause of familial Alzheimer's disease. Presenilin-1 knockout (PS1-/-) mice develop severe cortical dysplasia related to human type 2 lissencephaly. This overmigration syndrome has been attributed to the premature loss of Cajal-Retzius cells (CRcs), pioneer neurons required for the termination of radial neuronal migration. To elucidate the potential cellular mechanisms responsible for this premature neuronal loss, we investigated the morphological and electrophysiological properties of visually identified CRcs of wild-type (WT) and PS1-/- mouse brains at embryonic day 16.5. The density of CRcs was substantially reduced in the cerebral cortex of PS1-/-.…

Cell Adhesion Molecules NeuronalNerve Tissue ProteinsBiologyBicucullineMembrane PotentialsGABA AntagonistsMicemental disordersExcitatory Amino Acid AgonistsPresenilin-1medicineAnimalsneoplasms6-Cyano-7-nitroquinoxaline-23-dioneCerebral CortexMice KnockoutNeuronsMembrane potentialExtracellular Matrix ProteinsGABAA receptorStem CellsGeneral NeuroscienceSerine EndopeptidasesExcitatory Postsynaptic PotentialsMembrane ProteinsCortical dysplasiaBicucullineEmbryo Mammalianmedicine.diseaseImmunohistochemistryElectric Stimulationdigestive system diseasesnervous system diseasesCell biologyReelin ProteinElectrophysiologymedicine.anatomical_structure2-Amino-5-phosphonovaleratenervous systemCerebral cortexKnockout mouseExcitatory postsynaptic potentialExcitatory Amino Acid AntagonistsNeurosciencemedicine.drugEuropean Journal of Neuroscience
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Central cholinergic functions in human amyloid precursor protein knock-in/presenilin-1 transgenic mice.

2004

Alzheimer's disease is characterized by amyloid peptide formation and deposition, neurofibrillary tangles, central cholinergic dysfunction, and dementia; however, the relationship between these parameters is not well understood. We studied the effect of amyloid peptide formation and deposition on central cholinergic function in knock-in mice carrying the human amyloid precursor protein (APP) gene with the Swedish/London double mutation (APP-SL mice) which were crossbred with transgenic mice overexpressing normal (PS1wt) or mutated (M146L; PS1mut) human presenilin-1. APP-SLxPS1mut mice had increased levels of Abeta peptides at 10 months of age and amyloid plaques at 14 months of age while AP…

Genetically modified mousemedicine.medical_specialtyAmyloidMicrodialysisBACE1-ASScopolamineMice TransgenicPlaque AmyloidMuscarinic AntagonistsBiologyPresenilinAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseInternal medicinemental disordersmedicineAmyloid precursor proteinPresenilin-1AnimalsHumansNeuronsAmyloid beta-PeptidesBehavior AnimalGeneral NeuroscienceBrainMembrane ProteinsExtracellular FluidCholine acetyltransferaseAcetylcholineDisease Models AnimalEndocrinologyMutationbiology.proteinCholinergicAcetylcholinemedicine.drugNeuroscience
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Neuronal activity and secreted amyloid β lead to altered amyloid β precursor protein and presenilin 1 interactions.

2013

Deposition of amyloid β (Aβ) containing plaques in the brain is one of the neuropathological hallmarks of Alzheimer's disease (AD). It has been suggested that modulation of neuronal activity may alter Aβ production in the brain. We postulate that these changes in Aβ production are due to changes in the rate-limiting step of Aβ generation, APP cleavage by γ-secretase. By combining biochemical approaches with fluorescence lifetime imaging microscopy, we found that neuronal inhibition decreases endogenous APP and PS1 interactions, which correlates with reduced Aβ production. By contrast, neuronal activation had a two-phase effect: it initially enhanced APP-PS1 interaction leading to increased …

ImmunoprecipitationBlotting WesternEndogenyMice TransgenicCleavage (embryo)PresenilinArticlelcsh:RC321-571Amyloid beta-Protein PrecursorMiceAlzheimer Diseasemental disordersmedicinePresenilin-1Premovement neuronal activityAnimalsHumansImmunoprecipitationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryFeedback PhysiologicalNeuronsPresenilin 1Neuronal activityAmyloid beta-PeptidesChemistryP3 peptideNeurotoxicityAlzheimer's diseasemedicine.diseaseImmunohistochemistryCell biologyNeurologyBiochemistrynervous systemAlzheimer's diseaseAmyloid β precursor proteinFLIM (fluorescence lifetime imaging microscopy)Neurobiology of disease
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Low Density Lipoprotein Receptor-related Protein (LRP) Interacts with Presenilin 1 and Is a Competitive Substrate of the Amyloid Precursor Protein (A…

2005

Presenilin 1 (PS1) is a critical component of the gamma-secretase complex, which is involved in the cleavage of several substrates including the amyloid precursor protein (APP) and the Notch receptor. Recently, the low density receptor-related protein (LRP) has been shown to be cleaved by a gamma-secretase-like activity. We postulated that LRP may interact with PS1 and tested its role as a competitive substrate for gamma-secretase. In this report we show that LRP colocalizes and interacts with endogenous PS1 using coimmunoprecipitation and fluorescence lifetime imaging microscopy. In addition, we found that gamma-secretase active site inhibitors do not disrupt the interaction between LRP an…

ImmunoprecipitationNotch signaling pathwayMice TransgenicBinding CompetitiveBiochemistryPresenilinCell LineSubstrate SpecificityRats Sprague-DawleyAmyloid beta-Protein PrecursorMiceEndopeptidasesmental disordersPresenilin-1Amyloid precursor proteinAnimalsAspartic Acid EndopeptidasesHumansBinding siteMolecular BiologyBrain ChemistryBinding SitesbiologyChemistryMembrane ProteinsCell BiologyRatsnervous system diseasesCell biologyTransmembrane domainBiochemistryMultiprotein ComplexesLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Amyloid Precursor Protein SecretasesAmyloid precursor protein secretaseLow Density Lipoprotein Receptor-Related Protein-1Journal of Biological Chemistry
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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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Exercise and probiotics attenuate the development of Alzheimer's disease in transgenic mice: Role of microbiome

2018

Abstract It has been suggested that exercise training and probiotic supplementation could decelerate the progress of functional and biochemical deterioration in APP/PS1 transgenic mice (APP/PS1TG). APP/PS1TG mice were subjected to exercise training and probiotic treatments and functional, biochemical and microbiome markers were analyzed. Under these conditions the mice significantly outperformed controls on The Morris Maze Test, and the number of beta-amyloid plaques decreased in the hippocampus. B. thetaiotaomicron levels correlated highly with the results of the Morris Maze Test (p

Male0301 basic medicineGenetically modified mouseAgingalzheimer; exercise; microbiome; probioticsalzheimermicrobiomeMice TransgenicPlaque AmyloidDiseaseHippocampusBiochemistrylaw.inventionAmyloid beta-Protein PrecursorMice03 medical and health sciencesProbiotic0302 clinical medicineEndocrinologyAlzheimer DiseaselawPhysical Conditioning Animalmental disordersPresenilin-1GeneticsAnimalsHippocampus (mythology)MedicineMicrobiomeMolecular BiologyAmyloid beta-Peptidesexercisebusiness.industryMicrobiotaCell BiologyDisease Models Animal030104 developmental biologyprobioticsImmunologybusiness030217 neurology & neurosurgeryExperimental Gerontology
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