Search results for "tau protein"

showing 10 items of 48 documents

Stage-dependent agreement between cerebrospinal fluid proteins and FDG-PET findings in Alzheimer's disease.

2011

Cerebral hypometabolism and abnormal levels of amyloid beta (Aβ), total (t-tau) and phosphorylated tau (ptau) proteins in cerebrospinal fluid (CSF) are established biomarkers of Alzheimer's disease (AD). We examined the agreement between these biomarkers in a single center study of patients with AD of severity extending over a wide range. Forty seven patients (MMSE 21.4 ± 3.6, range 13-28 points) with incipient and probable AD underwent positron emission tomography with [18F]-fluorodeoxyglucose (FDG-PET) and lumbar puncture for CSF assays of Aβ1-42, p-tau181, and t-tau. All findings were classified as either positive or negative for AD. Statistical analyses were performed for the whole samp…

Malemedicine.medical_specialtyPathologyAmyloid betaApolipoprotein E4tau ProteinsNeuropsychological TestsGastroenterologySensitivity and SpecificityCerebrospinal fluidAlzheimer DiseaseFluorodeoxyglucose F18Internal medicinemental disordersmedicineDementiaHumansAgedRetrospective StudiesPsychiatric Status Rating ScalesAmyloid beta-Peptidesmedicine.diagnostic_testbiologyLumbar punctureNeurodegenerationCerebrospinal Fluid ProteinsMiddle Agedmedicine.diseasePeptide FragmentsNeurologyPositron emission tomographyArea Under CurvePositron-Emission Tomographybiology.proteinFemaleNeurology (clinical)Alzheimer's diseasePsychologyCognition DisordersKappaBiomarkersFollow-Up StudiesCurrent Alzheimer research
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Increased blood mercury levels in patients with Alzheimer's disease.

1998

Alzheimer's disease (AD) is a common neurodegenerative disorder that leads to dementia and death. In addition to several genetic parameters, various environmental factors may influence the risk of getting AD. In order to test whether blood levels of the heavy metal mercury are increased in AD, we measured blood mercury concentrations in AD patients (n = 33), and compared them to age-matched control patients with major depression (MD) (n = 45), as well as to an additional control group of patients with various non-psychiatric disorders (n = 65). Blood mercury levels were more than two-fold higher in AD patients as compared to both control groups (p = 0.0005, and p = 0.0000, respectively). In…

Malemedicine.medical_specialtyPathologyNeurologychemistry.chemical_elementtau ProteinsCentral nervous system diseaseDegenerative diseaseAlzheimer DiseaseInternal medicineBlood plasmamedicineDementiaHumansBiological PsychiatryAgedAged 80 and overDepressive DisorderAmyloid beta-PeptidesNeurodegenerationMercuryMiddle Agedmedicine.diseaseMercury (element)Psychiatry and Mental healthEndocrinologyNeurologychemistryLinear ModelsFemaleNeurology (clinical)Alzheimer's diseasePsychologyBiomarkersJournal of neural transmission (Vienna, Austria : 1996)
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CSF APPsα and Phosphorylated Tau Protein Levels in Mild Cognitive Impairment and Dementia of Alzheimer's Type

2008

We exploratively measured APPs alpha, a secreted fragment of the non-amyloidogenic cleavage of amyloid precursor protein via a-secretase, and tau protein phosphorylated at threonine 181 (p tau) in the cerebrospinal fluid of 10 patients with mild cognitive impairment, 20 patients with dementia of Alzheimer's type, and 10 controls. Cerebrospinal fluid APPs alpha and p tau levels were correlated with cognitive performance. P tau levels were significantly elevated in mild cognitive impairment and in patients with dementia of Alzheimer's type, APPs alpha levels were significantly reduced in patients with dementia of Alzheimer's type compared to the controls. APPs alpha levels were associated wit…

Malemedicine.medical_specialtyPathologyTau proteintau ProteinsNeuropsychological TestsSeverity of Illness IndexCerebrospinal fluidDegenerative diseaseAlzheimer DiseaseInternal medicineTask Performance and AnalysismedicineAmyloid precursor proteinHumansDementiaSex DistributionThreonineAgedAnalysis of VariancebiologyChemistrymedicine.diseasePsychiatry and Mental healthMemory Short-TermEndocrinologyMental Recallbiology.proteinPhosphorylationFemaleNeurology (clinical)Amyloid Precursor Protein SecretasesGeriatrics and GerontologyAlzheimer's diseaseCognition DisordersBiomarkersJournal of Geriatric Psychiatry and Neurology
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FDG-PET and CSF phospho-tau for prediction of cognitive decline in mild cognitive impairment

2006

Specific patterns of cortical glucose metabolism disturbances and increased CSF phospho-tau (p-tau(181)) concentrations could be demonstrated to predict cognitive decline and shift to dementia in amnestic mild cognitive impairment (MCI). But comparisons of both diagnostic tools have not been undertaken so far. The aim of the study was to compare (18)F-fluoro-2-deoxy-d-glucose positron emission tomography (FDG-PET) findings and CSF phospho-tau (p-tau(181)) measurements in the prediction of cognitive deterioration and conversion to dementia in MCI. During follow-up (mean 19 months) eight of 16 patients (50%) showed progressive cognitive decline, and four patients shifted to dementia. Patholog…

Malemedicine.medical_specialtyTau proteinNeuroscience (miscellaneous)tau ProteinsKaplan-Meier EstimateSeverity of Illness IndexStereotaxic TechniquesCentral nervous system diseaseImaging Three-DimensionalDegenerative diseaseFluorodeoxyglucose F18Internal medicinemental disordersSeverity of illnessImage Processing Computer-AssistedmedicineHumansDementiaRadiology Nuclear Medicine and imagingLongitudinal StudiesCognitive declineAgedPsychiatric Status Rating ScalesbiologyCognitive disorderPrognosismedicine.diseasePsychiatry and Mental healthPositron-Emission TomographyStereotaxic techniquebiology.proteinCardiologyDementiaFemaleCognition DisordersMental Status SchedulePsychologyNeuroscienceBiomarkersFollow-Up StudiesPsychiatry Research: Neuroimaging
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Glycogen synthase kinase 3β links neuroprotection by 17β-estradiol to key Alzheimer processes

2004

Estrogen exerts many of its receptor-mediated neuroprotective functions through the activation of various intracellular signal transduction pathways including the mitogen activating protein kinase (MAPK), phospho inositol-3 kinase and protein kinase C pathways. Here we have used a hippocampal slice culture model of kainic acid-induced neurotoxic cell death to show that estrogen can protect against oxidative cell death. We have previously shown that MAPK and glycogen synthase kinase-3beta (GSK-3beta) are involved in the cell death/cell survival induced by kainic acid. In this model and other cellular and in vivo models we have shown that estrogen can also cause the phosphorylation and hence …

Malemedicine.medical_specialtymedicine.drug_classBlotting WesternTetrazolium SaltsEstrogen receptorCell Counttau Proteinsmacromolecular substancesBiologyHippocampusRats Sprague-DawleyGlycogen Synthase Kinase 3MiceOrgan Culture TechniquesPregnancyGSK-3Internal medicineExcitatory Amino Acid AgonistsSerinemedicineAnimalsDrug InteractionsPhosphorylationProtein kinase AGSK3BCells CulturedProtein kinase CEstrogen receptor betaGlycogen Synthase Kinase 3 betaKainic AcidCell DeathEstradiolKinaseGeneral NeuroscienceAntibodies MonoclonalEmbryo MammalianImmunohistochemistryRatsCell biologyMice Inbred C57BLThiazolesEndocrinologyAnimals NewbornEstrogenTyrosineFemalePropidiumNeuroscience
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From Small Peptides to Large Proteins against Alzheimer'sDisease.

2022

Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the elderly. The two cardinal neuropathological hallmarks of AD are the senile plaques, which are extracellular deposits mainly constituted by beta-amyloids, and neurofibrillary tangles formed by abnormally phosphorylated Tau (p-Tau) located in the cytoplasm of neurons. Although the research has made relevant progress in the management of the disease, the treatment is still lacking. Only symptomatic medications exist for the disease, and, in the meantime, laboratories worldwide are investigating disease-modifying treatments for AD. In the present review, results centered on the use of peptides of different sizes invol…

NeuronsAmyloid beta-Peptidesamyloid-beta protein: amyloid fibrillationAlzheimer DiseaseTau proteinHumanstau ProteinsPlaque AmyloidNeurofibrillary TanglesMolecular BiologyBiochemistryAlzheimer’s diseaseAgedBiomolecules
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Immunohistochemical investigation of the brain of aged dogs. I. Detection of neurofibrillary tangles and of 4-hydroxynonenal protein, an oxidative da…

2001

In the aging dog brain lesions develop spontaneously. They share some morphological characteristics with those of Alzheimer 's disease in man. Diffuse and primitive plaques are well known, whereas neuritic plaques rarely develop. Neurofibrillary tangles have not been seen in the canine. The aim of the present investigation was to study major age-related changes of the dog's brain using paraffin sections with respect to cross-immunoreactivity of tau, A beta protein and other immunoreactive components including hydroxynonenal protein, which is a marker for oxidative damage. The occurrence of neurofibrillary tangles and of the protein tau therein was studied in serial brain sections of two dog…

Pathologymedicine.medical_specialtyAgingAmyloidmedicine.drug_classTau proteinModels NeurologicalNerve Tissue ProteinsPlaque AmyloidMonoclonal antibodymedicine.disease_causeDogsAlzheimer DiseaseInternal MedicinemedicineAnimalsHumansSenile plaquesDog DiseasesAldehydesbiologyChemistryBrainNeurofibrillary Tanglesmedicine.diseaseImmunohistochemistryOxidative StressPolyclonal antibodiesbiology.proteinImmunohistochemistryAlzheimer's diseaseOxidative stressAmyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis
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Molecular mechanisms linking amyloid β toxicity and Tau hyperphosphorylation in Alzheimer׳s disease

2015

Neurofibrillary tangles (aggregates of cytoskeletal Tau protein) and senile plaques (aggregates mainly formed by amyloid β peptide) are two landmark lesions in Alzheimer׳s disease. Some researchers have proposed tangles, whereas others have proposed plaques, as primary lesions. For a long time, these were thought of as independent mechanisms. However, experimental evidence suggests that both lesions are intimately related. We review here some molecular pathways linking amyloid β and Tau toxicities involving, among others, glycogen synthase kinase 3β, p38, Pin1, cyclin-dependent kinase 5, and regulator of calcineurin 1. Understanding amyloid β and Tau toxicities as part of a common pathophys…

Pathologymedicine.medical_specialtyAmyloid beta-PeptidesbiologyChemistryKinaseNeurodegenerationTau proteinBACE1-AStau Proteinsmedicine.diseaseProtein Aggregation PathologicalBiochemistryBiochemistry of Alzheimer's diseaseAlzheimer DiseaseGSK-3Physiology (medical)mental disordersmedicinebiology.proteinCancer researchPIN1HumansSenile plaquesPhosphorylationFree Radical Biology and Medicine
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Klinische Aspekte der "argyrophilic grain disease"

2000

Argyrophilic grain disease (AGD) is a frequently occurring degenerative illness of the aging human brain. It is accompanied by progressive pathological alterations of the cytsokeleton which are traceable to an abnormal phosphorylation of the microtubule associated tau protein. Histologically, it is possible with the help of suitable staining techniques to identify pathognomonic spindle-shaped cellular inclusions (argyrophilic grains). These cellular inclusions display a typical cortical as well as subcortical distribution pattern. The goal of the present study is the retrospective evaluation of the clinical findings from 53 individuals with neuropathologically demonstrable AGD-related chang…

Pathologymedicine.medical_specialtyNeurologybiologybusiness.industryTau proteinNeurodegenerationGeneral MedicineDiseaseHuman brainmedicine.diseasePsychiatry and Mental healthmedicine.anatomical_structureNeurologyPathognomonicbiology.proteinMedicineDementiaNeurology (clinical)businessPathologicalDer Nervenarzt
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Heterocyclic Scaffolds for the Treatment of Alzheimer's Disease

2016

Background: The treatment and diagnosis of Alzheimer’s Disease (AD) are two of the most urgent goals for research around the world. The cognitive decline is generally associated with the elevated levels of extracellular senile plaques, intracellular neurofibril- lary tangles (NFTs), and with a progressive shutdown of the cholinergic basal forebrain neurons transmission. Even if several key targets are under fervent investigation in the cure of AD, till now, the only approved therapeutic strategy is the treatment of symptoms by using cholinesterases inhibitors. It has been demonstrated that both acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) enzymes are not only responsible of…

Pathologymedicine.medical_specialtyTau proteinDisease010402 general chemistry01 natural scienceschemistry.chemical_compoundAlzheimer DiseaseHeterocyclic CompoundsDrug DiscoverymedicineAnimalsHumansSenile plaquesCognitive declineButyrylcholinesterasePharmacologybiologyMolecular Structure010405 organic chemistryChemistryAcetylcholinesterase0104 chemical sciencesbiology.proteinCholinergicNeuroscienceAmyloid precursor protein secretaseAlzheimer’s disease amyloid-peptide secretase acetylcholinesterase tau protein heterocycles
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