Search results for "Amyloid Precursor Protein"

showing 10 items of 134 documents

A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model

2004

Alzheimer disease (AD) is characterized by excessive deposition of amyloid beta-peptides (A beta peptides) in the brain. In the nonamyloidogenic pathway, the amyloid precursor protein (APP) is cleaved by the alpha-secretase within the A beta peptide sequence. Proteinases of the ADAM family (adisintegrin and metalloproteinase) are the main candidates as physiologically relevant alpha-secretases, but early lethality of knockout animals prevented a detailed analysis in neuronal cells. To overcome this restriction, we have generated transgenic mice that overexpress either ADAM10 or a catalytically inactive ADAM10 mutant. In this report we show that a moderate neuronal overexpression of ADAM10 i…

Genetically modified mousePathologymedicine.medical_specialtyAmyloidAmyloidADAM10BACE1-ASGene ExpressionMice TransgenicHippocampusArticleAmyloid beta-Protein PrecursorMiceAlzheimer DiseaseEndopeptidasesAmyloid precursor proteinmedicineAnimalsAspartic Acid EndopeptidasesHumansbiologybusiness.industryP3 peptideAmyloidosisGeneral Medicinemedicine.diseaseCell biologyEnzyme ActivationDisease Models AnimalCommentarybiology.proteinErratumAlzheimer's diseaseAmyloid Precursor Protein SecretasesbusinessAmyloid precursor protein secretaseJournal of Clinical Investigation
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Over-expression of two different forms of the α-secretase ADAM10 affects learning and memory in mice

2006

Members of the ADAM family (adisintegrin and metalloprotease) are the main candidates for physiologically relevant alpha-secretases. The alpha-secretase cleaves in the non-amyloidogenic pathway the amyloid precursor protein within the region of the Abeta peptides preventing their aggregation in the brain. The increase of alpha-secretase activity in the brain provides a plausible strategy to prevent Abeta formation. Concerning this possibility two transgenic mouse lines (FVB/N) have been created: mice over-expressing the bovine form of the alpha-secretase (ADAM10) and mice over-expressing an inactive form of the alpha-secretase (ADAM10-E348A-HA; ADAM10-dn). For behavioral examination a F1 ge…

Genetically modified mouseTransgeneMorris water navigation taskMice TransgenicAnxietyOpen fieldADAM10 ProteinMiceBehavioral NeuroscienceMemoryAmyloid precursor proteinAnimalsMaze LearningAnalysis of VarianceMotivationThigmotaxisBehavior AnimalbiologyWild typeMembrane ProteinsCell biologyMice Inbred C57BLADAM ProteinsExploratory Behaviorbiology.proteinAmyloid Precursor Protein SecretasesPsychologyAmyloid precursor protein secretaseNeuroscienceBehavioural Brain Research
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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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Effects of neuron-specific ADAM10 modulation in an in vivo model of acute excitotoxic stress.

2008

A disintegrin and metalloprotease (ADAM) 10 is the main candidate enzyme for the alpha-secretase processing of the amyloid precursor protein (APP). Neuron-specific ADAM10 overexpression proved beneficial in the APP[V717I] mutant Alzheimer mouse model [Postina R, Schroeder A, Dewachter I, Bohl J, Schmitt U, Kojro E, Prinzen C, Endres K, Hiemke C, Blessing M, Flamez P, Dequenne A, Godaux E, van Leuven F, Fahrenholz F (2004) A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model. J Clin Invest 113:1456-1464]. Since Alzheimer patients have a high prevalence for epileptic seizures, we investigated the effects of ADAM10 modula…

Genetically modified mousemedicine.medical_specialtyIndolesADAM10TransgeneExcitotoxicityMice Transgenicmedicine.disease_causeNeuroprotectionHippocampusADAM10 ProteinAmyloid beta-Protein PrecursorMiceLeucineSeizuresStress PhysiologicalInternal medicineGlial Fibrillary Acidic ProteinmedicineAmyloid precursor proteinAnimalsNeuroinflammationNeuronsAnalysis of VarianceKainic AcidbiologyCell DeathDose-Response Relationship DrugChemistryGeneral NeuroscienceNeurodegenerationMembrane ProteinsValinemedicine.diseaseADAM ProteinsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinAmyloid Precursor Protein SecretasesPlant LectinsNeuroscienceNeuroscience
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LRP1 modulates APP trafficking along early compartments of the secretory pathway

2008

The amyloid beta peptide (A beta) is a central player in Alzheimer's disease (AD) pathology. A beta liberation depends on APP cleavage by beta- and gamma-secretases. The low density lipoprotein receptor related protein 1 (LRP1) was shown to mediate APP processing at multiple steps. Newly synthesized LRP1 can interact with APP, implying an interaction between these two proteins early in the secretory pathway. We wanted to investigate whether LRP1 mediates APP trafficking along the secretory pathway, and, if so, whether it affects APP processing. Indeed, the early trafficking of APP within the secretory pathway is strongly influenced by its interaction with the C-terminal domain of LRP1. The …

GlycosylationAmyloid betaAmino Acid MotifsPlaque AmyloidCHO CellsSecretory pathwayTrafficinglcsh:RC321-571Amyloid beta-Protein PrecursorCricetulusAlzheimer DiseaseCricetinaemental disordersAmyloid precursor proteinAnimalsHumansReceptorlcsh:Neurosciences. Biological psychiatry. NeuropsychiatrySecretory pathwayNeuronsAmyloid beta-PeptidesbiologyLow density lipoprotein receptor related proteinBrainLRP1Cell CompartmentationProtein Structure TertiaryCell biologyProtein TransportNeurologyBiochemistryAlpha secretaseRetentionAmyloid precursor proteinLDL receptorbiology.proteinLiberationProtein Processing Post-TranslationalLow Density Lipoprotein Receptor-Related Protein-1Signal TransductionNeurobiology of Disease
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A Versatile Approach to CF3-Containing 2-Pyrrolidones by Tandem Michael Addition-Cyclization: Exemplification in the Synthesis of Amidine Class BACE1…

2015

The synthesis of new fluorinated pyrrolidones starting from unprotected amino esters and amino nitriles through a Michael addition-lactamization sequence is described. The resulting CF3 -containing building blocks, bearing a quaternary stereogenic center adjacent to the fluorinated group, have been converted into amino pyrrolidines that display potent β-secretase 1 (BACE1) inhibitory activity. This work constitutes an example of selective fluorination as a valid strategy for the modulation of physicochemical and biological properties of lead compounds in drug discovery.

Hydrocarbons FluorinatedMolecular StructureTandemAmino estersDrug discoveryStereochemistryOrganic ChemistryAmidinesStereoisomerismSequence (biology)General ChemistryCombinatorial chemistryPyrrolidinonesCatalysisStereocenterAmidinechemistry.chemical_compoundchemistryCyclizationBiological propertyDrug DiscoveryMichael reactionAspartic Acid EndopeptidasesAmyloid Precursor Protein SecretasesChemistry - A European Journal
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The neuroprotective actions of corticotropin releasing hormone

2005

Corticotropin-releasing hormone (CRH) modulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis, and has a key role in mediating neuroendocrine effects that occur in response to stressful stimuli. Disruption of the CRH system however has been shown to be closely associated with the progression of Alzheimer's disease (AD), and these observations prompted an investigation into the potential neuroprotective effects of the hormone. In addition to its regulatory affects on the molecular processes that underlie AD i.e., amyloid precursor protein (APP) processing and potentially tau phosphorylation, evidence is provided that the neuroprotective effects of CRH are mediated by a number…

Hypothalamo-Hypophyseal Systemendocrine systemAgingCorticotropin-Releasing HormonePituitary-Adrenal SystemBiochemistryNeuroprotectionCorticotropin-releasing hormoneAlzheimer DiseaseNeurotrophic factorsAmyloid precursor proteinAnimalsHumansReceptorMolecular BiologybiologyOxidative StressNeurologyApoptosisbiology.proteinPsychologyNeurosciencehormones hormone substitutes and hormone antagonistsIntracellularBiotechnologyHormoneAgeing Research Reviews
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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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Lack of APP and APLP2 in GABAergic Forebrain Neurons Impairs Synaptic Plasticity and Cognition.

2020

AbstractAmyloid-β precursor protein (APP) is central to the pathogenesis of Alzheimer’s disease, yet its physiological functions remain incompletely understood. Previous studies had indicated important synaptic functions of APP and the closely related homologue APLP2 in excitatory forebrain neurons for spine density, synaptic plasticity, and behavior. Here, we show that APP is also widely expressed in several interneuron subtypes, both in hippocampus and cortex. To address the functional role of APP in inhibitory neurons, we generated mice with a conditional APP/APLP2 double knockout (cDKO) in GABAergic forebrain neurons using DlxCre mice. These DlxCre cDKO mice exhibit cognitive deficits i…

InterneuronCognitive NeuroscienceLong-Term PotentiationSpatial LearningHippocampusAction PotentialsInhibitory postsynaptic potentialHippocampusNesting Behavior03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorMice0302 clinical medicineCognitionProsencephalonAmyloid precursor proteinmedicineAnimalsGABAergic NeuronsCA1 Region Hippocampal030304 developmental biologySpatial MemoryMice Knockout0303 health sciencesNeuronal PlasticitybiologyPyramidal CellsExcitatory Postsynaptic PotentialsLong-term potentiationmedicine.anatomical_structurenervous systemInhibitory Postsynaptic PotentialsSynaptic plasticityForebrainExcitatory postsynaptic potentialbiology.proteinNeuroscience030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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Melittin Modulates Keratinocyte Function through P2 Receptor-dependent ADAM Activation

2012

Melittin, the major component of the bee venom, is an amphipathic, cationic peptide with a wide spectrum of biological properties that is being considered as an anti-inflammatory and anti-cancer agent. It modulates multiple cellular functions but the underlying mechanisms are not clearly understood. Here, we report that melittin activates disintegrin-like metalloproteases (ADAMs) and that downstream events likely contribute to the biological effects evoked by the peptide. Melittin stimulated the proteolysis of ADAM10 and ADAM17 substrates in human neutrophil granulocytes, endothelial cells and murine fibroblasts. In human HaCaT keratinocytes, melittin induced shedding of the adhesion molecu…

KeratinocytesCell SurvivalBlotting WesternADAM17 ProteinP2 receptorBiologyModels Biologicalcomplex mixturesBiochemistryMelittinCell LineADAM10 ProteinMicechemistry.chemical_compoundTransactivationAdenosine TriphosphateAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesReceptorMolecular BiologyCells CulturedMice KnockoutDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionPurinergic receptorHEK 293 cellstechnology industry and agricultureMembrane ProteinsCell BiologyFibroblastsCadherinsEmbryo MammalianMelittenCell biologyErbB ReceptorsADAM ProteinsHaCaTHEK293 CellschemistryPhosphorylationlipids (amino acids peptides and proteins)Receptors Purinergic P2X7Amyloid Precursor Protein SecretasesJournal of Biological Chemistry
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