Search results for "Degenerative disease"

showing 10 items of 250 documents

Association between the polymorphisms of TLR4 and CD14 genes and Alzheimer's disease.

2008

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. Inflammation plays a key role in AD and dissecting the genetics of inflammation may provide an answer to the possible treatment. Hence, the better understanding of different molecular and cellular inflammatory mechanisms is crucial for complete knowledge of AD pathophysiology, and for its prevention and drug therapy. Accordingly, in the present study we evaluated whether the pro-inflammatory polymorphisms of lipopolysaccaride-receptors, +896A/G Toll-Like Receptor (TLR4) and -260C/T CD14, are risk factors for AD. The study included both 626 AD …

MaleALZHEIMER'S DISEASEINFLAMMATIONINNATE IMMUNITYTLR4CD14Lipopolysaccharide ReceptorsInflammationSingle-nucleotide polymorphismDiseaseSystemic inflammationPolymorphism Single NucleotideSeverity of Illness IndexDegenerative diseaseINFLAMMATIONAlzheimer DiseaseRisk FactorsDrug DiscoverymedicineDementiaSNPHumansTLR4AgedPharmacologyAged 80 and overbusiness.industryMiddle Agedmedicine.diseaseToll-Like Receptor 4ItalyALZHEIMER'S DISEASEImmunologyINNATE IMMUNITYFemalemedicine.symptomAlzheimer's diseasebusinessCD14
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Comparison of motor strategies in sit-to-stand and back-to-sit motions between healthy and Alzheimer’s disease elderly subjects

2005

We studied the kinematics of shoulder displacement during sit-to-stand and back-to-sit in 6 healthy elderly subjects and six elderly subjects with mild to moderate Alzheimer's disease in order to elucidate the impact of Alzheimer's disease on motor planning and control processes. During sit-to-stand, Alzheimer's disease subjects reduced their forward displacement and started their upward displacement earlier than healthy elderly subjects. Furthermore, shoulder path curvatures were more pronounced for upward compared with downward displacement in healthy elderly group, in contrast with Alzheimer's disease group. Temporal analysis found that: 1) for both groups, profiles of velocity of sit-to…

MaleAgingmedicine.medical_specialtyTime FactorsMovementAccelerationPostureDiseaseEfferent PathwaysCentral nervous system diseaseDegenerative diseasePhysical medicine and rehabilitationAlzheimer DiseaseReference ValuesUpward displacementmedicinePostural BalanceHumansPostural BalanceAgedAged 80 and overLegMovement DisordersSit to standGeneral NeuroscienceBrainsocial sciencesmedicine.diseaseSurgeryArmFemaleAnalysis of varianceAlzheimer's diseasePsychologyPsychomotor PerformanceNeuroscience
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Association between apolipoprotein E epsilon4 allele and apathy in probable Alzheimer's disease.

2006

OBJECTIVE: There have been inconclusive results to date on the association between the Apolipoprotein E (ApoE) genotype and neuropsychiatric symptoms (NPS) in Alzheimer's disease (AD). We investigated whether ApoE epsilon4 allele is associated with NPS in probable AD. METHOD: Data for 197 subjects with probable AD were analysed. The Neuropsychiatric Inventory was used to evaluate the frequency and severity of NPS. Multiple logistic regression models were used to test the association between ApoE genotype and NPS in AD. RESULTS: The ApoE epsilon3/3 genotype was present in 52.3%, epsilon3/4 in 44.1%, and epsilon4/4 in 3.6% of patients. ApoE epsilon4 carriers showed a higher frequency of apath…

MaleApolipoprotein EGenotypeApolipoprotein E4DiseaseNeuropsychological TestsSeverity of Illness IndexApolipoproteins EDegenerative diseaseAlzheimer Diseasemental disordersGenotypemedicineHumansDementiaApathyAllelebehavioural symptomAllelesAgedapolipoprotein EMood DisordersAlzheimer's diseasemedicine.diseasePsychiatry and Mental healthImmunologyFemalelipids (amino acids peptides and proteins)Settore MED/26 - NeurologiaAlzheimer's diseasemedicine.symptomPsychologyNeurosciencelogistic modelsdementia
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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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Complications in Craniovertebral Junction Instrumentation: Hardware Removal Can Be Associated with Long-Lasting Stability. Personal Experience

2017

Background The causes of craniovertebral junction (CVJ) instabilities include trauma, rheumatological diseases, tumors, infections, congenital malformations, and degenerative disease processes; these complex pathologies often require CVJ instrumentation. Hardware complications were analyzed in a personal series of 48 treated patients. In light of the analysis of very unusual radiological and clinical findings, the authors tried to better investigate the related mechanisms and to reach possible useful conclusions. Methods In a series of 48 patients who underwent CVJ instrumentation and fusion procedures in our Institution, we describe three cases of hardware failure, due to: (1) infection; (…

MaleBone ScrewsOccipito-cervical fusionOccipito cervical fusion030218 nuclear medicine & medical imagingPostoperative Complications0302 clinical medicineDegenerative diseaseMedicineAxis Cervical VertebraBone infections; Craniovertebral junction; Occipito-cervical fusion; Screwing; Wiring; Surgery; Neurology (clinical)EncephaloceleMedulla OblongataWiringSettore MED/27 - NeurochirurgiaCraniovertebral junctionCongenital malformationsMiddle AgedDecompression SurgicalMagnetic Resonance ImagingBone infectionsProsthesis FailureAtlanto-Axial JointRadiological weaponScrewingComputer hardwareBone WiresJoint InstabilityLong lastingProsthesis-Related InfectionsAdolescentAntineoplastic AgentsBone NeoplasmsCongenital Abnormalities03 medical and health sciencesOdontoid ProcessHumansInstrumentation (computer programming)Device RemovalRadiotherapybusiness.industrymedicine.diseaseRadiographyAtlanto-Occipital JointSpinal FusionSurgeryNeurology (clinical)Tomography X-Ray Computedbusiness030217 neurology & neurosurgeryPlasmacytoma
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A restricted population of CB1 cannabinoid receptors with neuroprotective activity.

2014

The CB1 cannabinoid receptor, the main molecular target of endocannabinoids and cannabis active components, is the most abundant G protein-coupled receptor in the mammalian brain. Of note, CB1 receptors are expressed at the synapses of two opposing (i.e., GABAergic/inhibitory and glutamatergic/excitatory) neuronal populations, so the activation of one and/or another receptor population may conceivably evoke different effects. Despite the widely reported neuroprotective activity of the CB1 receptor in animal models, the precise pathophysiological relevance of those two CB1 receptor pools in neurodegenerative processes is unknown. Here, we first induced excitotoxic damage in the mouse brain b…

MaleCannabinoid receptorPopulationNeurotoxinsExcitotoxicityGlutamic AcidBiologymedicine.disease_causeNeuroprotectionGlutamatergicMiceOrgan Culture TechniquesReceptor Cannabinoid CB1medicineAnimalsHumansGABAergic NeuronsReceptoreducationCaenorhabditis elegans ProteinsAgedCerebral CortexMice KnockoutNeuronseducation.field_of_studyMultidisciplinaryIntegrasesmusculoskeletal neural and ocular physiologyNeurodegenerative DiseasesBiological SciencesMiddle AgedReceptors GABA-AEndocannabinoid systemCorpus Striatumnervous systemGABAergiclipids (amino acids peptides and proteins)FemaleNeurosciencepsychological phenomena and processesEndocannabinoidsSynaptosomesProceedings of the National Academy of Sciences of the United States of America
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Beta-adrenoceptor density and subtype distribution in cerebellum and hippocampus from patients with Alzheimer's disease

1993

beta-Adrenoceptor density and beta 1- and beta 2-subtype distribution were examined in hippocampi and cerebella from patients with Alzheimer's disease (AD/SDAT). Tissues from age-, sex and post-mortem delay matched non-demented patients served as controls. The total beta-adrenoceptor density as evaluated in saturation experiments with the hydrophilic radioligand [3H]CGP 12177 was higher in hippocampal (36-39 fmol/mg protein) than cerebellar tissues (20-21 fmol/mg), however, no differences were found in either brain region between AD/SDAT patients and controls. Subtype distribution using the highly selective beta 1-adrenoceptor antagonist CGP 20712A revealed a slightly higher proportion of b…

MaleCerebellummedicine.medical_specialtyAdrenergic beta-AntagonistsHippocampal formationTritiumBinding CompetitiveHippocampusPropanolaminesAdenylyl cyclaseBasal (phylogenetics)chemistry.chemical_compoundDegenerative diseaseAlzheimer DiseaseCerebellumInternal medicineReceptors Adrenergic betamedicineHumansHippocampus (mythology)AgedAged 80 and overPharmacologybusiness.industryImidazolesAntagonistGeneral MedicineMiddle Agedmedicine.diseaseKineticsmedicine.anatomical_structureEndocrinologychemistryDementiaFemaleAlzheimer's diseasebusinessNaunyn-Schmiedeberg's Archives of Pharmacology
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rTMS of supplementary motor area modulates therapy-induced dyskinesias in Parkinson disease

2005

The neural mechanisms and circuitry involved in levodopa-induced dyskinesia are unclear. Using repetitive transcranial magnetic stimulation (rTMS) over the supplementary motor area (SMA) in a group of patients with advanced Parkinson disease, the authors investigated whether modulation of SMA excitability may result in a modification of a dyskinetic state induced by continuous apomorphine infusion. rTMS at 1 Hz was observed to markedly reduce drug-induced dyskinesias, whereas 5-Hz rTMS induced a slight but not significant increase.

MaleDyskinesia Drug-InducedApomorphinemedicine.medical_treatmentDopamineNeurological disorderNOCentral nervous system diseaseDegenerative diseasemental disordersNeural PathwaysmedicineHumansAgedSupplementary motor areaDyskinesiabusiness.industryDyskinesia Drug-Induced; Treatment Outcome; Male; Middle Aged; Female; Humans; Parkinson Disease; Motor Cortex; Recovery of Function; Apomorphine; Dopamine Agonists; Neural Pathways; Aged; Transcranial Magnetic Stimulation; DopamineMotor CortexParkinson DiseaseRecovery of FunctionMiddle Agedmedicine.diseaseSMA*Transcranial Magnetic Stimulationnervous system diseasesTranscranial magnetic stimulationApomorphinemedicine.anatomical_structureTreatment OutcomeDyskinesiaDrug-InducedDopamine AgonistsFemaleSettore MED/26 - NeurologiaNeurology (clinical)medicine.symptombusinessNeurosciencemedicine.drug
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The role of mind theory in patients affected by neurodegenerative disorders and impact on caregiver burden

2020

Abstract Background Theory of Mind (ToM) is defined as the ability to understand mental and emotional state. This ability is assessed also in neurodegenerative disease. Few studies have investigated the impact that social cognition of patients could have on caregiver burden. The aim of this study was to investigate a possible correlation in level of social cognition impairment between patients with different neurodegenerative disorders and their caregivers with possible impact on caregivers burden. Methods we enrolled 48 patients with dementia divided in different groups: Fronto-Temporal Dementia (FTD), Alzheimer Disease (AD), and Mild Cognitive Impairment (MCI) and also the three groups of…

MaleEmotionsTheory of MindDiseaseFronto-temporal dementia03 medical and health sciences0302 clinical medicineSocial cognitionAlzheimer DiseasePhysiology (medical)Theory of mindmental disordersActivities of Daily Livingmedicine80 and overDementiaHumansIn patientCognitive DysfunctionAlzheimer disease; Caregiver; Dementia; Fronto-temporal dementia; Mild cognitive impairment; Theory of mind; Activities of Daily Living; Aged; Aged 80 and over; Alzheimer Disease; Caregivers; Cognitive Dysfunction; Emotions; Female; Frontotemporal Dementia; Humans; Male; Middle Aged; Neurodegenerative Diseases; Theory of MindAgedAged 80 and overbusiness.industryMild cognitive impairmentNeurodegenerative DiseasesGeneral MedicineCaregiver burdenMiddle Agedmedicine.diseaseCaregiverDistressNeurologyCaregivers030220 oncology & carcinogenesisFrontotemporal DementiaSurgeryDementiaFemaleNeurology (clinical)Alzheimer's diseasebusiness030217 neurology & neurosurgeryClinical psychology
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Association between the HFE mutations and unsuccessful ageing: a study in Alzheimer's disease patients from Northern Italy

2003

Mutations in the class I-like Major Histocompatibility Complex gene HFE are associated with hereditary hemochromatosis (HH), a disorder caused by excessive iron uptake. Three common mutations have been found: C282Y, H63D, and S65C. Moreover, several studies have suggested that HFE mutations may be involved in several age-related chronic diseases such as Alzheimer's disease (AD) and coronary heart disease, but apparently paradoxically also with longevity. In particular, in AD, patients carrying the H63D allele have been suggested to have a mean age at onset of 72 vs. 77 years for those who were homozygous for the wild-type allele. Thus, it seems that H63D mutations may anticipate sporadic AD…

MaleHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAgingDiseasemedicine.disease_causeDegenerative diseaseGene FrequencyAlzheimer DiseaseGenotypeHumansPoint MutationMedicineAlleleHemochromatosis ProteinHemochromatosisAgedGeneticsMutationbusiness.industryHistocompatibility Antigens Class IHomozygoteMembrane Proteinsnutritional and metabolic diseasesMiddle Agedmedicine.diseaseItalyHereditary hemochromatosisFemaleAlzheimer's diseasebusinessDevelopmental BiologyMechanisms of Ageing and Development
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