Search results for "tau protein"

showing 10 items of 48 documents

Molecular properties underlying regional vulnerability to Alzheimer’s disease pathology

2018

Amyloid deposition and neurofibrillary degeneration in Alzheimer's disease specifically affect discrete neuronal systems, but the underlying mechanisms that render some brain regions more vulnerable to Alzheimer's disease pathology than others remain largely unknown. Here we studied molecular properties underlying these distinct regional vulnerabilities by analysing Alzheimer's disease-typical neuroimaging patterns of amyloid deposition and neurodegeneration in relation to regional gene expression profiles of the human brain. Graded patterns of brain-wide vulnerability to amyloid deposition and neurodegeneration in Alzheimer's disease were estimated by contrasting multimodal amyloid-sensiti…

Male0301 basic medicinePathologyphysiology [Amyloidogenic Proteins]genetics [Transcriptome]genetics [Alzheimer Disease]Cohort StudiesTranscriptomepathology [Alzheimer Disease]metabolism [Amyloidogenic Proteins]methods [Magnetic Resonance Imaging]0302 clinical medicinepathology [Brain]Gene expressiongenetics [Genetic Predisposition to Disease]Aged 80 and overmethods [Positron-Emission Tomography]NeurodegenerationBrainNeurofibrillary TanglesHuman brainMagnetic Resonance Imagingmetabolism [Neurofibrillary Tangles]medicine.anatomical_structureFemalemethods [Neuroimaging]Alzheimer's Disease Neuroimaging InitiativeAmyloidmedicine.medical_specialtyAmyloidmetabolism [Amyloid beta-Peptides]Amyloidogenic ProteinsNeuroimagingtau ProteinsBiology03 medical and health sciencesAlzheimer DiseasemedicineHumansDementiaGenetic Predisposition to Diseaseddc:610metabolism [Amyloid]AgedAmyloid beta-PeptidesCyclin-dependent kinase 5medicine.diseasemetabolism [tau Proteins]030104 developmental biologyPositron-Emission Tomographypathology [Neurofibrillary Tangles]Neurology (clinical)Transcriptome030217 neurology & neurosurgeryBrain
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Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer's disease: histotopographical correlation with amyloid pl…

1999

Impairment of cholinergic transmission and decreased numbers of nicotinic binding sites are well-known features accompanying the cognitive dysfunction seen in Alzheimer's disease (AD). In order to elucidate the underlying cause of this cholinoceptive dysfunction, the expression of two pharmacologically different nicotinic acetylcholine receptor (nAChR) subunits (alpha4, alpha7) was studied in the cerebral cortex of Alzheimer patients as compared to controls. Patch-clamp recordings of 14 dissociated neurons of control cortices showed responses suggesting the existence of alpha4- and alpha7-containing functional nAChRs in the human cortex. In cortices of Alzheimer patients and controls, the p…

MaleAmyloidTau proteinPlaque Amyloidtau ProteinsReceptors Nicotiniccomplex mixturesAlzheimer DiseaseCortex (anatomy)mental disordersmedicineHumansProtein IsoformsRNA MessengerPhosphorylationAgedAged 80 and overCerebral CortexNeuronsAmyloid beta-PeptidesbiologyGeneral NeuroscienceHuman brainFrontal LobeNicotinic acetylcholine receptormedicine.anatomical_structureNicotinic agonistnervous systemCerebral cortexbiology.proteinCholinergicFemalesense organsNeuroscienceEuropean Journal of Neuroscience
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Apolipoprotein E isoforms and the development of low and high Braak stages of Alzheimer's disease-related lesions

1999

In recent research, apolipoprotein-E (apoE) polymorphism has been shown to influence the formation of neurofibrillary changes and the accumulation of beta/A4-amyloid, the histopathological hallmarks of Alzheimer's disease (AD). Clinical studies associate the apoE allele epsilon4 with earlier onset of the disease, although the clinical speed of progression remains unchanged. Time course estimates have also provided evidence which indicates that the clinical phase of AD constitutes only 10-20% of the total time span needed for the development of this slowly progressing degenerative brain disorder. Due to the lack of reliable clinical tests for the detection of pre-symptomatic stages of AD, we…

MaleApolipoprotein Emedicine.medical_specialtyPathologyGenotypeApolipoprotein BApolipoprotein E2Apolipoprotein E4Apolipoprotein E3tau ProteinsNeuropathologyPathology and Forensic MedicineCellular and Molecular NeuroscienceApolipoproteins EDegenerative diseaseIsomerismAlzheimer DiseaseInternal medicineGenotypemedicineHumansAlleleAllelesBrain ChemistryAmyloid beta-PeptidesPolymorphism GeneticbiologyBrainNeurofibrillary TanglesNeurofibrillary tangleMiddle Agedmedicine.diseaseEndocrinologyDisease Progressionbiology.proteinFemaleNeurology (clinical)Alzheimer's diseaseActa Neuropathologica
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Genetic linkage of autosomal dominant progressive supranuclear palsy to 1q31.1

2005

Progressive supranuclear palsy (PSP) is a disorder of unknown pathogenesis. Familial clusters of PSP have been reported related to mutations of protein tau. We report the linkage of a large Spanish family with typical autosomal dominant PSP to a new locus in chromosome 1. Four members of this family had typical PSP, confirmed by neuropathology in one case. At least five ancestors had similar disease. Other members of the family have incomplete phenotypes. The power of the linkage analysis was increased by detecting presymptomatic individuals with 18F-fluoro-dopa and 18F-deoxyglucose positron emission tomography. We screened the human genome with 340 polymorphic markers and we enriched the a…

MaleGenetic LinkageTau proteinLocus (genetics)NeuropathologyProgressive supranuclear palsyGenetic linkagemedicineHumansAgedBrain ChemistryGeneticsbiologyPutamenChromosomeDNAMiddle Agedmedicine.diseaseeye diseasesDihydroxyphenylalaninePedigreeChromosome 17 (human)GlucosePhenotypeNeurologyChromosomes Human Pair 1Genetic markerPositron-Emission Tomographybiology.proteinFemaleSupranuclear Palsy ProgressiveNeurology (clinical)Caudate NucleusLod ScoreRadiopharmaceuticalsAnnals of Neurology
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Frontotemporal dementia: the post-tau era.

2006

As scientists have begun to decipher the molecular genetic bases of hereditary frontotemporal dementia (FTD), it has become clear that the biology of these human neurodegenerative diseases has a complexity not previously suspected. FTD has been found to be linked to several chromosomal loci including those in chromosome 9, chromosome 17, and chromosome 3. The article by Guyant-Marechal et al. in this issue of Neurology reports the clinical, pathologic, and molecular characteristics of a form of FTD associated with inclusion body myopathy and Paget disease of the bone observed in members of two families and expands our knowledge on genetically determined FTD.1 The disorder is associated with…

MaleHeterozygoteMultiple Organ FailureDNA Mutational AnalysisChromosome 9Cell Cycle ProteinsChromosome Disorderstau ProteinsBiologyRisk AssessmentMyositis Inclusion BodyExonRisk FactorsValosin Containing ProteinmedicinePrevalenceHumansGenetic Predisposition to DiseaseGeneRetrospective StudiesGeneticsAdenosine TriphosphatasesIncidenceChromosomeSyndromeMiddle Agedmedicine.diseaseOsteitis DeformansPhenotypePedigreeChromosome 17 (human)Chromosome 3MutationDementiaFemaleNeurology (clinical)FranceFrontotemporal dementiaNeurology
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Limited agreement between biomarkers of neuronal injury at different stages of Alzheimer's disease

2013

Abstract New diagnostic criteria for Alzheimer's disease (AD) treat different biomarkers of neuronal injury as equivalent. Here, we quantified the degree of agreement between hippocampal volume on structural magnetic resonance imaging, regional glucose metabolism on positron emission tomography, and levels of phosphorylated tau in cerebrospinal fluid (CSF) in 585 subjects from all phases of the AD Neuroimaging Initiative. The overall chance-corrected agreement was poor (Cohen κ, 0.24–0.34), in accord with a high rate of conflicting findings (26%–41%). Neither diagnosis nor APOE e4 status significantly influenced the distribution of agreement between the biomarkers. The degree of agreement t…

MalePathologymedicine.medical_specialtyEpidemiologytau ProteinsHippocampus03 medical and health sciencesCellular and Molecular NeuroscienceApolipoproteins E0302 clinical medicineAtrophyCerebrospinal fluidDevelopmental NeuroscienceNeuroimagingAlzheimer DiseaseFluorodeoxyglucose F18medicineHumansDementiaCognitive DysfunctionAged030304 developmental biology0303 health sciencesChi-Square Distributionmedicine.diagnostic_testHealth PolicyMiddle Agedmedicine.diseasePsychiatry and Mental healthPositron emission tomographyPositron-Emission TomographyBiomarker (medicine)FemaleNeurology (clinical)AtrophyGeriatrics and GerontologyAlzheimer's diseaseMental Status SchedulePsychologyChi-squared distributionBiomarkers030217 neurology & neurosurgeryAlzheimer's & Dementia
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Neocortical Variation of Abeta Load in Fully Expressed, Pure Alzheimer's Disease

2010

The relationship between amyloid-beta (A beta) deposition and tau-related neurofibrillary changes is a key issue in the pathogenesis of Alzheimer's disease (AD). The aim of this study was to investigate the extent and cortical distribution of A beta and tau pathology, their mutual links and their correlation with the duration of the disease in thirty-nine patients with fully expressed AD. By tau immunohistochemistry, we identified different patterns of distribution of neurofibrillary changes that were ascribed to Braak stage V and VI. The disease duration was longer in patients at Braak stage VI than in those at V. Morphometric analysis carried out in several neocortical areas demonstrated …

MalePathologymedicine.medical_specialtyTau proteinNeocortextau ProteinsPathogenesisSuperior temporal gyrusAlzheimer Diseasemental disordersmedicineHumansSenile plaquesAgedAged 80 and overNeocortexAmyloid beta-PeptidesbiologyGeneral NeuroscienceGeneral MedicinePsychiatry and Mental healthClinical Psychologymedicine.anatomical_structureGene Expression RegulationCerebral cortexbiology.proteinDisease ProgressionFemaleGeriatrics and GerontologyPrimary motor cortexPsychologyNeuroscienceBraak staging
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Association of elevated phospho-tau levels with alzheimer-typical 18F-Fluoro-2-Deoxy-D-Glucose positron emission tomography findings in patients with…

2003

Abstract Background Mild cognitive impairment is considered to be a transitional stage between normal aging and dementia. Phosphorylated tau protein in cerebrospinal fluid and even more decrements of cerebral glucose metabolism in parietal, temporal, or cingulate regions have shown favorable specificity for the diagnosis of Alzheimer dementia and could be useful supplementary tools to determine Alzheimer pathology in early stages. Methods We measured cerebrospinal fluid tau phosphorylated at threonine 181 protein, cerebrospinal fluid total tau, and cerebral glucose metabolism using 18F-fluoro-2-deoxy-D-glucose positron emission tomography in 16 patients with mild cognitive impairment and ag…

MalePathologymedicine.medical_specialtyTau proteintau ProteinsNeuropsychological TestsStatistics NonparametricCentral nervous system diseasechemistry.chemical_compoundCerebrospinal fluidAlzheimer DiseaseFluorodeoxyglucose F18Predictive Value of Testsmental disordersmedicineHumansDementiaPhosphorylationBiological PsychiatryAgedAged 80 and overBrain ChemistryBrain Mappingmedicine.diagnostic_testbiologybusiness.industryMiddle Agedmedicine.diseaseGlucosechemistryPositron emission tomographyCase-Control Studiesbiology.proteinBiomarker (medicine)FemaleAlzheimer's diseaseCognition Disorders2-Deoxy-D-glucosebusinessTomography Emission-ComputedBiological Psychiatry
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Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer's disease patients: A neuroimaging biomarker of the disease.

2017

Purpose The objective of this study was to correlate the presence and distribution of cerebral microbleeds in Alzheimer’s disease patients with cerebrospinal fluid biomarkers (amyloid-beta and phosphorylated tau 181 protein levels) and cognitive decline by using susceptibility-weighted imaging magnetic resonance sequences at 1.5 T. Material and methods Fifty-four consecutive Alzheimer’s disease patients underwent brain magnetic resonance imaging at 1.5 T to assess the presence and distribution of cerebral microbleeds on susceptibility-weighted imaging images. The images were analyzed in consensus by two neuroradiologists, each with at least 10 years’ experience. Dementia severity was assess…

MalePathologymedicine.medical_specialtytau ProteinsDisease030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineCerebrospinal fluidNeuroimagingAlzheimer DiseasemedicineHumansRadiology Nuclear Medicine and imagingAlzheimer's disease; Cerebral microbleeds; magnetic resonance imaging; susceptibility-weighted imaging; Radiology Nuclear Medicine and Imaging; Neurology (clinical)AgedCerebral HemorrhageAmyloid beta-Peptidesmedicine.diagnostic_testbusiness.industryCerebral microbleedBrainMagnetic resonance imagingGeneral MedicineAlzheimer's diseaseMagnetic Resonance Imagingsusceptibility-weighted imagingSusceptibility weighted imagingBiomarker (medicine)FemaleNeurology (clinical)business030217 neurology & neurosurgeryBiomarkersThe neuroradiology journal
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Cerebrospinal fluid tau protein is not a biological marker in amyotrophic lateral sclerosis.

2009

Background:  Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder leading to progressive motor neuron cell death. Etiopathogenesis is still imperfectly known and much effort have been undertaken to find a biological marker that could help in the early diagnosis and in the monitoring of disease progression. Cerebrospinal fluid (CSF) concentrations of tau, an axonal microtubule-associated protein, have been measured in ALS with levels found increased in some studies and unchanged in others. Methods:  Total CSF tau level was assayed in a population of ALS patients (n = 57) and controls (n = 110) using a specific ELISA method. Results:  No significant differences in the median CS…

MaleProgrammed cell deathPathologymedicine.medical_specialtyTau proteinPopulationEnzyme-Linked Immunosorbent Assaytau Proteinscerebrospinal fluidtau proteinCerebrospinal fluiddisease progressionHumansMedicineamyotrophic lateral sclerosiAmyotrophic lateral sclerosisElisa methodeducationAgededucation.field_of_studybiologybusiness.industryAmyotrophic Lateral SclerosisDisease progressionMiddle AgedMotor neuronmedicine.diseasemedicine.anatomical_structureNeurologybiology.proteinamyotrophic lateral sclerosis cerebrospinal fluid disease progression tau proteinFemaleSettore MED/26 - NeurologiaNeurology (clinical)businessBiomarkers
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