Search results for "degenerative"

showing 10 items of 334 documents

Cofilin and Neurodegeneration: New Functions for an Old but Gold Protein

2021

Cofilin is an actin-binding protein that plays a major role in the regulation of actin dynamics, an essential cellular process. This protein has emerged as a crucial molecule for functions of the nervous system including motility and guidance of the neuronal growth cone, dendritic spine organization, axonal branching, and synaptic signalling. Recently, other important functions in cell biology such as apoptosis or the control of mitochondrial function have been attributed to cofilin. Moreover, novel mechanisms of cofilin function regulation have also been described. The activity of cofilin is controlled by complex regulatory mechanisms, with phosphorylation being the most important, since t…

0301 basic medicineDendritic spine organizationCellMotilityNeurosciences. Biological psychiatry. NeuropsychiatryReviewmacromolecular substancescofilinBiologyenvironment and public health03 medical and health sciences0302 clinical medicinemedicineneurodegenerative diseasescofilin–actin rodsGeneral Neurosciencemitochondrial fissionNeurodegenerationapoptosisCofilinmedicine.diseaseCell biologymicrotubule instability030104 developmental biologymedicine.anatomical_structurePhosphorylationMitochondrial fission030217 neurology & neurosurgeryFunction (biology)RC321-571Brain Sciences
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Honey and obesity-related dysfunctions: a summary on health benefits

2020

Honey is a natural product, containing flavonoids and phenolic acids, appreciated for its therapeutic abilities since ancient times. Although the bioactive potential is linked to the composition, that is variable depending on mainly the botanical origin, honey has antioxidant and anti-inflammatory properties. Therefore, honey, administered alone or in combination with conventional therapy, might result useful in the management of chronic diseases that are commonly associated with oxidative stress and inflammation state. Obesity is a metabolic disorder characterized by visceral adiposity. The adipose tissue becomes hypertrophic and undergoes hyperplasia, resulting in a hypoxic environment, o…

0301 basic medicineHealth StatusEndocrinology Diabetes and MetabolismClinical BiochemistryAnti-Inflammatory AgentsAdipose tissueGlycemic Controlmedicine.disease_causeBioinformaticsBiochemistryAntioxidants03 medical and health sciences0302 clinical medicineHydroxybenzoatesAnimalsHumansMedicineObesityNeurodegenerationMolecular BiologyGlycemicFlavonoidsInflammationMetabolic SyndromeHyperplasiaNutrition and Dieteticsmedicine.diagnostic_testbusiness.industryfungiMetabolic disorderNeurodegenerationPolyphenolsfood and beveragesNeurodegenerative DiseasesHoneymedicine.diseaseObesityOxidative Stress030104 developmental biologyDiabetes Mellitus Type 2HypertensionOxidative streInsulin ResistanceMetabolic syndromebusinessLipid profile030217 neurology & neurosurgeryOxidative stressThe Journal of Nutritional Biochemistry
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The Role of the Multifunctional BAG3 Protein in Cellular Protein Quality Control and in Disease

2017

In neurons, but also in all other cells the complex proteostasis network is monitored and tightly regulated by the cellular protein quality control (PQC) system. Beyond folding of newly synthesized polypeptides and their refolding upon misfolding the PQC also manages the disposal of aberrant proteins either by the ubiquitin-proteasome machinery or by the autophagic-lysosomal system. Aggregated proteins are primarily degraded by a process termed selective macroautophagy (or aggrephagy). One such recently discovered selective macroautophagy pathway is mediated by the multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3). Under acute stress and during cellular aging, BAG3 in …

0301 basic medicineHuntingtinSOD1AggrephagyReviewBAG3lcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceUbiquitinselective macroautophagymedicineprotein quality controllcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyproteostasisbiologyBAG3NeurodegenerationAutophagymedicine.diseaseCell biology030104 developmental biologyProteostasisneurodegenerative disordersbiology.proteinNeuroscienceFrontiers in Molecular Neuroscience
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Influence of gut microbiota on neuropsychiatric disorders

2017

The last decade has witnessed a growing appreciation of the fundamental role played by an early assembly of a diverse and balanced gut microbiota and its subsequent maintenance for future health of the host. Gut microbiota is currently viewed as a key regulator of a fluent bidirectional dialogue between the gut and the brain (gut-brain axis). A number of preclinical studies have suggested that the microbiota and its genome (microbiome) may play a key role in neurodevelopmental and neurodegenerative disorders. Furthermore, alterations in the gut microbiota composition in humans have also been linked to a variety of neuropsychiatric conditions, including depression, autism and Parkinson’s dis…

0301 basic medicineHypothalamo-Hypophyseal SystemGut–brain axisPituitary-Adrenal SystemDiseaseGut floraBioinformaticsdigestive systemEpigenesis Genetic03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansBrain-gut axisMicrobiomePsychiatric conditionsbiologyMicrobiotaGastrointestinal MicrobiomeGastroenterologyBrainNeurodegenerative DiseasesMinireviewsGeneral MedicineDNA MethylationFecal Microbiota TransplantationMental illnessmedicine.diseasebiology.organism_classificationGastrointestinal MicrobiomeTransplantationDisease Models Animal030104 developmental biologyNeurodevelopmental DisordersDysbiosisMental healthMicrobiomeDysbiosisStress Psychological030217 neurology & neurosurgeryWorld Journal of Gastroenterology
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Neurodegeneration in tauopathies and synucleinopathies.

2016

International audience; While increasing life expectancy is a major achievement, the global aging of societies raises a number of medical issues, such as the development of age-related disorders, including neurodegenerative diseases. The three main disease groups constituting the majority of neurodegenerative diseases are tauopathies, alpha-synucleinopathies and diseases due to repetitions of glutamine (including Huntington's disease). In each neurodegenerative disease, the accumulation of one or more aggregated proteins has been identified as the molecular signature of the disease (as seen, for example, in Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies, amyotrophic lat…

0301 basic medicineLewy Body DiseaseParkinson's disease[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyParkinson's diseaseDementia with Lewy bodiesMédecine humaine et pathologieDiseaseBioinformatics03 medical and health scienceschemistry.chemical_compound0302 clinical medicineParkinsonian Disorders[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMedicineDementiaHumansCytoskeletonSynucleinopathiesAlpha-synucleinInclusion Bodiesbusiness.industryDementia with Lewy bodiesNeurodegenerative diseasesNeurodegenerationassociationBrainNeurodegenerative DiseasesAlzheimer's diseasemedicine.disease3. Good health030104 developmental biologyNeurologychemistryTauopathies[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyNerve Degenerationalpha-SynucleinDementiapathologyNeurology (clinical)businessNeuroscience030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyFrontotemporal dementiadementiaRevue neurologique
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Relationship Between Body Mass Index, ApoE4 Status, and PET-Based Amyloid and Neurodegeneration Markers in Amyloid-Positive Subjects with Normal Cogn…

2018

Body weight loss in late-life is known to occur at a very early stage of Alzheimer's disease (AD). Apolipoprotein E4 (ApoE4) represents a major genetic risk factor for AD and is linked to an increased cortical amyloid-β (Aβ) accumulation. Since the relationship between body weight, ApoE4, and AD pathology is poorly investigated, we aimed to evaluate whether ApoE4 allelic status modifies the association of body mass index (BMI) with markers of AD pathology. A total of 368 Aβ-positive cognitively healthy or mild cognitive impaired subjects had undergone [18F]-AV45-PET, [18F]-FDG-PET, and T1w-MRI examinations. Composite cortical [18F]-AV45 uptake and [18F]-FDG uptake in posterior cingulate cor…

0301 basic medicineMaleApolipoprotein E4Body Mass Index0302 clinical medicineCognitionWeight lossCognitive declineAniline CompoundsGeneral NeuroscienceNeurodegenerationBrainCognitionNeurodegenerative DiseasesGeneral MedicinePsychiatry and Mental healthClinical PsychologyEthylene GlycolsFemalemedicine.symptommedicine.medical_specialtyAmyloidHeterozygote03 medical and health sciencesFluorodeoxyglucose F18Internal medicinemental disordersWeight LossmedicineHumansCognitive DysfunctionEffects of sleep deprivation on cognitive performanceAdaptor Proteins Signal TransducingAgedbusiness.industryZebrafish Proteinsmedicine.diseaseCortex (botany)Repressor Proteins030104 developmental biologyEndocrinologyGlucosePosterior cingulatePositron-Emission TomographyGeriatrics and GerontologyRadiopharmaceuticalsbusinessNeuroscienceBody mass index030217 neurology & neurosurgeryFollow-Up StudiesJournal of Alzheimer's disease : JAD
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Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification

2020

International audience; Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromo…

0301 basic medicineMaleCerebellumPathology[SDV]Life Sciences [q-bio]recessive brain calcificationMice0302 clinical medicineCognitive declineAge of OnsetChildGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSBrain Diseasesprimary familial brain calcificationMalalties neurodegenerativesBrainFahr diseaseCalcinosisOCLNNeurodegenerative DiseasesHuman brainMiddle AgedPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structureKnockout mouseFemalemedicine.symptomAdultmedicine.medical_specialtyAdolescentGenes RecessiveNeuropathologyBiologyCalcificacióCalcification03 medical and health sciencesBasal Ganglia DiseasesReportGeneticsmedicineAnimalsHumansAllelesSLC20A2Cerebellar ataxiaknock out mouse modelmedicine.diseaseJAM2030104 developmental biologyFahr disease; familial idiopathic basal ganglia calcification; JAM2; JAM3; knock out mouse model; MYORG; OCLN; primary familial brain calcification; recessive brain calcification; SLC20A2familial idiopathic basal ganglia calcificationJAM3MYORGXenotropic and Polytropic Retrovirus ReceptorCell Adhesion Molecules030217 neurology & neurosurgeryCalcification
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Amyotrophic lateral sclerosis modifies progenitor neural proliferation in adult classic neurogenic brain niches.

2017

Background Adult neurogenesis persists through life at least in classic neurogenic niches. Neurogenesis has been previously described as reduced in neurodegenerative diseases. There is not much knowledge about is adult neurogenesis is or not modified in amyotrophy lateral sclerosis (ALS). All previous publications has studied the ALS SOD1 (superoxide dismutase) transgenic mouse model. The purpose of this study is to examine the process of adult neurogenesis in classic niches (subventricular zone [SVZ] and subgranular zone [SGZ] of the dentate gyrus) in patients with amyotrophic lateral sclerosis (ALS), both with (ALS-FTD) and without associated frontotemporal dementia (FTD). Methods We stud…

0301 basic medicineMalePathologymedicine.medical_specialtyDoublecortin ProteinTDP-43NeurogenesisSOD1Subventricular zoneAdult neurogenesislcsh:RC346-429Subgranular zone03 medical and health sciences0302 clinical medicineNeuroblastNeural Stem CellsLateral VentriclesMedicineHumansAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemAgedAged 80 and overbusiness.industryDentate gyrusNeurogenesisAmyotrophic Lateral SclerosisNeurodegenerative diseasesBrainGeneral MedicineMiddle Agedmedicine.diseaseNeural stem cellnervous system diseases030104 developmental biologymedicine.anatomical_structurenervous systemFrontotemporal DementiaFemaleNeurology (clinical)business030217 neurology & neurosurgeryResearch ArticleBMC neurology
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Genetic and constitutional factors are major contributors to substantia nigra hyperechogenicity

2017

9 páginas, 2 figuras, 4 tablas

0301 basic medicineMalemedicine.medical_specialtyMovement disordersScienceSubstantia nigraDiseaseComorbidityArticle03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansGenetic Predisposition to DiseaseFamily historyAmyotrophic lateral sclerosisPsychiatryGenetic Association StudiesGenetic testingAgedUltrasonographyMultidisciplinarymedicine.diagnostic_testbusiness.industryQCase-control studyRNeurodegenerative DiseasesMiddle Agedmedicine.diseaseComorbiditySubstantia Nigra030104 developmental biologyCase-Control StudiesMutationMedicineFemalemedicine.symptombusiness030217 neurology & neurosurgeryBiomarkers
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DeepWAS: Multivariate genotype-phenotype associations by directly integrating regulatory information using deep learning

2020

Genome-wide association studies (GWAS) identify genetic variants associated with traits or diseases. GWAS never directly link variants to regulatory mechanisms. Instead, the functional annotation of variants is typically inferred by post hoc analyses. A specific class of deep learning-based methods allows for the prediction of regulatory effects per variant on several cell type-specific chromatin features. We here describe “DeepWAS”, a new approach that integrates these regulatory effect predictions of single variants into a multivariate GWAS setting. Thereby, single variants associated with a trait or disease are directly coupled to their impact on a chromatin feature in a cell type. Up to…

0301 basic medicineMultivariate analysisGene ExpressionGenome-wide association studyBiochemistry0302 clinical medicineGenotypeMedicine and Health SciencesBiology (General)0303 health sciencesDNA methylationEcologyChromosome BiologyNeurodegenerative DiseasesGenomicsChromatinChromatinNucleic acidsNeurologyComputational Theory and MathematicsModeling and SimulationDNA methylationTraitEpigeneticsDNA modificationFunction and Dysfunction of the Nervous SystemChromatin modificationResearch ArticleMultiple SclerosisQH301-705.5Quantitative Trait LociImmunologySingle-nucleotide polymorphismComputational biologyBiologyQuantitative trait locusPolymorphism Single NucleotideAutoimmune DiseasesMolecular Genetics03 medical and health sciencesCellular and Molecular NeuroscienceDeep LearningGenome-Wide Association StudiesGeneticsHumansGeneMolecular BiologyGenetic Association StudiesEcology Evolution Behavior and Systematics030304 developmental biologyGenetic associationBiology and Life SciencesComputational BiologyHuman GeneticsCell BiologyDNAGenome AnalysisDemyelinating Disorders030104 developmental biologyGenetic LociMultivariate AnalysisClinical ImmunologyClinical Medicine030217 neurology & neurosurgeryGenome-Wide Association StudyPLOS Computational Biology
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