Search results for "Neuronal cultures"

showing 4 items of 4 documents

Design and synthesis of new trehalose-conjugated pentapeptides as inhibitors of Aβ(1-42) fibrillogenesis and toxicity

2009

Aggregation of the amyloid A? peptide and its accumulation into insoluble deposits (plaques) are believed to be the main cause of neuronal dysfunction associated with Alzheimer's disease (AD); small molecules that can interfere with the A? amyloid fibril formation are therefore of interest for a potential therapeutic strategy. Three new trehalose-conjugated peptides of the well known ?-sheet breaker peptide iA?5p,were synthesized. The disaccharide was covalently attached to different sites of the LPFFD peptide chain, i.e. at the N-terminus, C-terminus or at the Asp side chain. CD spectroscopy in different solvents was used to assess changes in the peptide conformation of these compounds. Th…

AmyloidCell SurvivalPeptideMicroscopy Atomic ForceBiochemistryMass Spectrometrychemistry.chemical_compoundbeta-sheet breaker peptideStructural BiologySFMmental disordersDrug DiscoveryAnimalsbeta-sheet breaker peptidesMolecular BiologyCells CulturedChromatography High Pressure LiquidtrehaloseCerebral CortexPharmacologychemistry.chemical_classificationthioflavin Tbeta-amyloidOrganic ChemistryP3 peptideFibrillogenesisGeneral MedicineTrehaloseSmall moleculeGlycopeptideNeuronal culturesRatsPeptide Conformationneuronal cultureBiochemistrychemistryMolecular MedicineAmyloid-betaPeptidesJournal of Peptide Science
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Missense variants in DPYSL5 cause a neurodevelopmental disorder with corpus callosum agenesis and cerebellar abnormalities

2021

International audience; The collapsin response mediator protein (CRMP) family proteins are intracellular mediators of neurotrophic factors regulating neurite structure/spine formation and are essential for dendrite patterning and directional axonal pathfinding during brain developmental processes. Among this family, CRMP5/DPYSL5 plays a significant role in neuronal migration, axonal guidance, dendrite outgrowth, and synapse formation by interacting with microtubules. Here, we report the identification of missense mutations in DPYSL5 in nine individuals with brain malformations, including corpus callosum agenesis and/or posterior fossa abnormalities, associated with variable degrees of intel…

Models MolecularMale0301 basic medicineHydrolases[SDV]Life Sciences [q-bio]Hippocampal formationMedical and Health Sciences0302 clinical medicineNeurodevelopmental disorderTubulinModelsNeurotrophic factorsCerebellumIntellectual disability2.1 Biological and endogenous factorsMissense mutationAetiologyChilddendrite branchingGenetics (clinical)de novo missense variantsPediatricGenetics & HeredityDPYSL5Biological Sciences[SDV] Life Sciences [q-bio]corpus callosum agenesisMental HealthChild PreschoolNeurologicalFemaleMicrotubule-Associated ProteinsAdultNeuriteIntellectual and Developmental Disabilities (IDD)primary neuronal culturesMutation MissenseBiologyYoung Adult03 medical and health sciencesRare DiseasesMediatorReportIntellectual DisabilityGeneticsmedicineHumansPreschoolCorpus Callosum Agenesisbrain malformationNeurosciencesMolecularmedicine.diseaseneurodevelopmental disorderBrain Disorders030104 developmental biologyNeurodevelopmental DisordersMutationMissenseAgenesis of Corpus CallosumNeuroscience030217 neurology & neurosurgery
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Designing trehalose-conjugated peptides for the inhibition of Alzheimer’s Aβ oligomerization and neurotoxicity

2008

Neurotoxicity Alzheimer Amyloidsbeta-sheet breaker peptides • amyloid-beta • trehalose • SFM • neuronal cultures • thioflavin T
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Designing trehalose-conjugated peptide inhibitors for the oligomerization and toxicity of Alzheimer’s Aβ 11th Naples

2008

beta-sheet breaker peptides • amyloid-beta • trehalose • SFM • neuronal cultures • thioflavin T
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