Search results for "ALZHEIMER'S DISEASE"

showing 10 items of 301 documents

Structure and Synaptic Function of Metal Binding to the Amyloid Precursor Protein and its Proteolytic Fragments

2017

Alzheimer’s disease (AD) is ultimately linked to the Amyloid Precursor Protein (APP). However, current research reveals an important synaptic function of APP and APP-like proteins (APLP1 and 2). In this context various neurotrophic and neuroprotective functions have been reported for the APP proteolytic fragments sAPPα, sAPPβ, and the monomeric amyloid-beta peptide (Aβ). APP is a metalloprotein and binds copper and zinc ions. Synaptic activity correlates with a release of these ions into the synaptic cleft and dysregulation of their homeostasis is linked to different neurodegenerative diseases. Metal binding to APP or its fragments affects its structure and its proteolytic cleavage and ther…

0301 basic medicineSynaptic cleftamyloid precursor protein (APP)Context (language use)ReviewNeurotransmission03 medical and health sciencesCellular and Molecular Neurosciencemental disordersAmyloid precursor proteinsynaptic transmissionAPLP1Molecular BiologybiologyChemistryzincP3 peptideCell biologyBiochemistry of Alzheimer's disease030104 developmental biologyAlpha secretaseBiochemistrycopperbiology.proteinAlzheimer’s diseaseNeuroscienceFrontiers in Molecular Neuroscience
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Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer’s disease

2018

Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or …

0301 basic medicineTime Factorsmedicine.medical_treatmentHippocampusCell CountPharmacologymedicine.disease_causeHippocampuslcsh:RC346-429Superoxide Dismutase-10302 clinical medicineNeuroinflammationNF-kBMicrogliaGeneral NeuroscienceMicrofilament ProteinsROSPro-inflammatory cytokineIFNβ1amedicine.anatomical_structureCytokineNeurologyIL-10CytokinesFemalemedicine.symptomAlzheimer's diseaseInterferon beta-1aPro-inflammatory cytokinesImmunologyAβ 1-42InflammationProinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceHippocampuAlzheimer DiseaseGlial Fibrillary Acidic ProteinmedicineAnimalsAβ1-42Rats WistarSODMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationInflammationAmyloid beta-PeptidesNeuroscience (all)Superoxide Dismutasebusiness.industryResearchCalcium-Binding ProteinsRecognition Psychologymedicine.diseasePeptide FragmentsRatsDisease Models Animal030104 developmental biologyLipid PeroxidationCognition DisordersReactive Oxygen Speciesbusiness030217 neurology & neurosurgeryOxidative stressJournal of Neuroinflammation
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MicroRNAs miR-19, miR-340, miR-374 and miR-542 regulate MID1 protein expression.

2018

The MID1 ubiquitin ligase activates mTOR signaling and regulates mRNA translation. Misregulation of MID1 expression is associated with various diseases including midline malformation syndromes, cancer and neurodegenerative diseases. While this indicates that MID1 expression must be tightly regulated to prevent disease states specific mechanisms involved have not been identified. We examined miRNAs to determine mechanisms that regulate MID1 expression. MicroRNAs (miRNA) are small non-coding RNAs that recognize specific sequences in their target mRNAs. Upon binding, miRNAs typically downregulate expression of these targets. Here, we identified four miRNAs, miR-19, miR-340, miR-374 and miR-542…

0301 basic medicineUntranslated regionSmall interfering RNAPhysiologymetabolism [Microtubule Proteins]Alzheimer's DiseaseBiochemistryImmune PhysiologyMedicine and Health SciencesSmall interfering RNAsmetabolism [Transcription Factors]3' Untranslated RegionsImmune System ProteinsMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionMessenger RNAQRNuclear ProteinsNeurodegenerative DiseasesTranslation (biology)EnzymesUbiquitin ligaseCell biologyNucleic acidsNeurologyMicrotubule ProteinsMedicineOxidoreductasesLuciferasemetabolism [Nuclear Proteins]Research ArticleScienceUbiquitin-Protein LigasesImmunologyTransfectionResearch and Analysis MethodsReal-Time Polymerase Chain ReactionAntibodies03 medical and health sciencesMental Health and PsychiatrymicroRNAGeneticsHumansddc:610Non-coding RNAMolecular Biology TechniquesMolecular BiologyMessenger RNABiology and life sciencesThree prime untranslated regionHEK 293 cellsProteinsGene regulationphysiology [MicroRNAs]MicroRNAs030104 developmental biologyHEK293 CellsEnzymologybiology.proteinRNAProtein TranslationDementiaGene expressionTranscription FactorsMid1 protein human
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Changes in Serine Racemase-Dependent Modulation of NMDA Receptor: Impact on Physiological and Pathological Brain Aging

2018

International audience; The N-methyl-D-Aspartate glutamate receptors (NMDARs) are pivotal for the functional and morphological plasticity that are required in neuronal networks for efficient brain activities and notably for cognitive-related abilities. Because NMDARs are heterogeneous in subunit composition and associated with multiple functional regulatory sites, their efficacy is under the tonic influence of numerous allosteric modulations, whose dysfunction generally represents the first step generating pathological states. Among the enzymatic candidates, serine racemase (SR) has recently gathered an increasing interest considering that it tightly regulates the production of D-serine, an…

0301 basic medicine[SDV]Life Sciences [q-bio]Allosteric regulation[SHS.PSY]Humanities and Social Sciences/PsychologyglutamateDiseaseReviewBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)BiochemistryNMDA receptors[SHS.PSY] Humanities and Social Sciences/Psychology03 medical and health sciences0302 clinical medicineserine racemasemedicineMolecular BiosciencesAmyotrophic lateral sclerosislong term potentiationMolecular BiologyPathologicallcsh:QH301-705.5ComputingMilieux_MISCELLANEOUS[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceagingGlutamate receptorLong-term potentiationAlzheimer's diseasemedicine.diseaseMESH: NMDA receptors serine racemase aging Alzheimer’s disease D-serine long term potentiation glutamate[SDV] Life Sciences [q-bio]030104 developmental biologylcsh:Biology (General)d-serineSerine racemaseNMDA receptor[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neuroscience030217 neurology & neurosurgeryFrontiers in Molecular Biosciences
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Physiological Functions of the β-Site Amyloid Precursor Protein Cleaving Enzyme 1 and 2

2017

BACE1 was discovered as the β-secretase for initiating the cleavage of amyloid precursor protein (APP) at the β-secretase site, while its close homology BACE2 cleaves APP within the β-amyloid (Aβ) domain region and shows distinct cleavage preferences in vivo. Inhibition of BACE1 proteolytic activity has been confirmed to decrease Aβ generation and amyloid deposition, and thus specific inhibition of BACE1 by small molecules is a current focus for Alzheimer’s disease therapy. While BACE1 inhibitors are being tested in advanced clinical trials, knowledge regarding the properties and physiological functions of BACE is highly important and this review summarizes advancements in BACE1 research ov…

0301 basic medicineamyloid plaquessecretaseReviewamyloid precursor proteinBiology03 medical and health sciencesCellular and Molecular Neurosciencemental disordersAmyloid precursor proteinaspartic proteaseBACE substratesGlucose homeostasisMolecular Biologychemistry.chemical_classificationNeurogenesisBACE2P3 peptideBACE1Biochemistry of Alzheimer's disease030104 developmental biologyEnzymechemistryBiochemistrySynaptic plasticitybiology.proteinAmyloid precursor protein secretaseAlzheimer’s diseaseNeuroscienceFrontiers in Molecular Neuroscience
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Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC

2019

Seventy years of research on Western Pacific amyotrophic lateral sclerosis and Parkinsonism-dementia Complex (ALS/PDC) have provided invaluable data on the etiology, molecular pathogenesis and latency of this disappearing, largely environmental neurodegenerative disease. ALS/PDC is linked to genotoxic chemicals (notably methylazoxymethanol, MAM) derived from seed of the cycad plant (Cycas spp.) that were used as a traditional food and/or medicine in all three disease-affected Western Pacific populations. MAM, nitrosamines and hydrazines generate methyl free radicals that damage DNA (in the form of O6-methylguanine lesions) that can induce mutations in cycling cells and degenerative changes …

0301 basic medicineamyotrophic lateral sclerosisDNA damageDiseaseBiologylcsh:RC346-429Environmental - originProgressive supranuclear palsy03 medical and health sciences0302 clinical medicineHypothesis and TheorymedicinenitrosaminesAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemhydrazinesprogressive supranuclear palsymedicine.diseaseatypical parkinsonism030104 developmental biologyBrain degenerationNeurologyImmunologyEtiologycycad methylazoxymethanol and L-BMAADNA damageNeurology (clinical)Alzheimer's diseaseAlzheimer disease030217 neurology & neurosurgeryFrontiers in Neurology
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Vitamin D and the nervous system

2019

Objective: to summarise the activities that Vitamin D (VD) carries out in the brain and to clarify the potential role of VD in neurological diseases. Methods: a literature research has been performed in Pubmed using the following keywords: 'Vitamin D', 'nervous system', 'brain'. Results: the studies reviewed show that VD contributes to cerebral activity in both embryonic and adult brain, helping the connectivity of neural circuits responsible for locomotor, emotional and reward-dependent behavior. Low VD serum levels have been found in patients affected by Alzheimer Disease, Parkinson Disease, Multiple Sclerosis, Autism Spectrum Disorders, Sleep Disorders and Schizophrenia. Discussion: find…

0301 basic medicinecognitionMultiple SclerosisbrainDiseaseBioinformaticsCalcitriol receptorNervous Systemvitamin D deficiency03 medical and health sciences0302 clinical medicineMultiple SclerosimedicineVitamin D and neurologyHumansVitamin DVDRNeurodegenerative Diseasebusiness.industryMultiple sclerosisNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseVitamin D Deficiencybehaviour030104 developmental biologyNeurologySchizophreniaAutismReceptors CalcitriolNeurology (clinical)Alzheimer's diseasebusiness030217 neurology & neurosurgeryHuman
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Dysregulation of C-X-C motif ligand 10 during aging and association with cognitive performance

2017

International audience; Chronic low-grade inflammation during aging (inflammaging) is associated with cognitive decline and neurodegeneration; however, the mechanisms underlying inflammaging are unclear. We studied a population (n = 361) of healthy young and old adults from the MyoAge cohort. Peripheral levels of C-X-C motif chemokine ligand 10 (CXCL10) was found to be higher in older adults, compared with young, and negatively associated with working memory performance. This coincided with an age-related reduction in blood DNA methylation at specific CpGs within the CXCL10 gene promoter. In vitro analysis supported the role of DNA methylation in regulating CXCL10 transcription. A polymorph…

0301 basic medicinegamma interferon inducible protein 10genomic DNAAlzheimerin tautiEpigenesis GeneticCohort StudiesCXCL10 geneCognitionsingle nucleotide polymorphismcognitive defectCognitive declineAged 80 and overCerebral Cortexeducation.field_of_studyprefrontal cortexDNA methylationGeneral NeuroscienceadultNeurodegenerationneurodegenerationta3141U937 CellsMethylationta3142Alzheimer's diseasecohort analysisDNA-metylaatioagedfemalepriority journalepigenetiikkaDNA methylationAlzheimer's diseaseAlzheimer diseasetranscription regulationAlzheimer’s diseasekognitiiviset taidotmedicine.medical_specialty[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]in vitro studyAdolescentheredityPopulationBiologyArticleworking memoryYoung Adult03 medical and health sciencesCognitive agingpromoter regionmaleMemoryInternal medicineJournal Articlemedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansCXCL10controlled studyEpigeneticshumanbrain levelNeurodegenerationeducationepigeneticscognitive aginghuman cellagingdisease associationmedicine.diseasemajor clinical studyInflammagingChemokine CXCL10gamma interferon inducible protein 10; genomic DNA adult; age; aged; aging; Alzheimer disease; Article; brain level; cognitive defect; cohort analysis; controlled study; CpG island; CXCL10 gene; disease association; DNA methylation; epigenetics; female; heredity; human; human cell; in vitro study; inflammation; major clinical study; male; prefrontal cortex; priority journal; promoter region; single nucleotide polymorphism; transcription regulation; working memory; Alzheimer's disease; Cognitive aging; DNA methylation; Epigenetics; Inflammaging; Neurodegeneration030104 developmental biologyEndocrinologyikääntyminenageinflammationNerve DegenerationCpG islandinflammagingNeurology (clinical)Geriatrics and GerontologyHeLa CellsDevelopmental BiologyNeurobiology of Aging
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Regulation of Alpha-Secretase ADAM10 In vitro and In vivo: Genetic, Epigenetic, and Protein-Based Mechanisms

2017

ADAM10 (A Disintegrin and Metalloproteinase 10) has been identified as the major physiological alpha-secretase in neurons, responsible for cleaving APP in a non-amyloidogenic manner. This cleavage results in the production of a neuroprotective APP-derived fragment, APPs-alpha, and an attenuated production of neurotoxic A-beta peptides. An increase in ADAM10 activity shifts the balance of APP processing towards APPs-alpha and protects the brain from amyloid deposition and disease. Thus, increasing ADAM10 activity has been proposed an attractive target for the treatment of neurodegenerative diseases and it appears to be timely to investigate the physiological mechanisms regulating ADAM10 expr…

0301 basic medicinepromoterADAM10agingADAM10ReviewBiologyAlzheimer's diseaseNeuroprotectionspineProtein–protein interaction03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologyAlpha secretaseIn vivoalpha-secretasetranscription factorsmicroRNAmouse modelsEpigeneticsNeuroscienceTranscription factorMolecular BiologyNeuroscienceFrontiers in Molecular Neuroscience
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The Metalloprotease Meprin β Is an Alternative β-Secretase of APP

2017

The membrane bound metalloprotease meprin β is important for collagen fibril assembly in connective tissue formation and for the detachment of the intestinal mucus layer for proper barrier function. Recent proteomic studies revealed dozens of putative new substrates of meprin β, including the amyloid precursor protein (APP). It was shown that APP is cleaved by meprin β in distinct ways, either at the β-secretase site resulting in increased levels of Aβ peptides, or at the N-terminus releasing 11 kDa, and 20 kDa peptide fragments. The latter event was discussed to be rather neuroprotective, whereas the ectodomain shedding of APP by meprin β reminiscent to BACE-1 is in line with the amyloid h…

0301 basic medicineproteolysisADAM10ProteolysisN-terminal truncated AβReview03 medical and health sciencesCellular and Molecular Neuroscienceshedding0302 clinical medicinemedicineAmyloid precursor proteinMolecular BiologyMetalloproteinasemedicine.diagnostic_testbiologyChemistryCell adhesion moleculemeprin βSheddaseBiochemistry of Alzheimer's disease030104 developmental biologyBiochemistryEctodomainbiology.proteinAPP030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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