Search results for "ALZHEIMER"

showing 10 items of 706 documents

Inflammation, genes and zinc in Alzheimer's disease.

2007

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. AD has been linked to inflammation and metal biological pathway. Neuro-pathological hallmarks are senile plaques, resulting from the accumulation of several proteins and an inflammatory reaction around deposits of amyloid, a fibrillar protein, Abeta, product of cleavage of a much larger protein, the beta-amyloid precursor protein (APP) and neurofibrillary tangles. Amyloid deposition, due to the accumulation of Abeta peptide, is the main pathogenetic mechanism. Inflammation clearly occurs in pathologically vulnerable regions of AD and several i…

BACE1-ASInflammationBiologyModels BiologicalBiological pathwayApolipoproteins EAlzheimer Diseasemental disordersmedicineAnimalsHumansSenile plaquesInflammation genes zinc Alzheimer's diseaseSettore MED/04 - Patologia GeneraleInflammationAmyloid beta-PeptidesGeneral NeuroscienceP3 peptidemedicine.diseasePhenotypeBiochemistry of Alzheimer's diseaseZincCholesterolImmunologyCytokinesNeurology (clinical)Alzheimer's diseasemedicine.symptomBrain research reviews
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Involvment of docosanoïc acid (C22=0), and of very long chain fatty acids (tetracosanoïc acid (C24=0), hexacosanoïc acid (C26=0) in Alzheimer's disea…

2013

In the brain and in the plasma of patients with Alzheimer’s disease (AD), marked accumulation of C22:0 and of very long chain fatty acids (C24:0 ; C26:0) have been reported. Important decreases of docosahexaenoic acid (DHA; C22:6 n-3) have also been described as well as quantitative and qualitative modifications of plasmalogens. Altogether, these lipid modifications suggest an implication of peroxisomal metabolism disorders in the physiopathology of AD. Therefore, the biological activities of C22:0, C24:0 and C26:0 have been studied on human neuronal cells SK-N-BE. On these cells, the lipotoxicity of fatty acids (C22:0, C24:0 and C26:0) leads to various cellular modifications: topographical…

Biomarqueurs[SDV.SA] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyHexacosanoic acid (C26:0)Acide hexacosanoique (C26:0)Souris transgénique APP PS1 ΔE9Transgenic mouse APP PS1 ΔE9PeroxisomeMaladie d’AlzheimerAcides gras à très longue chaîneVery long chain fatty acidsLipotoxicitéTetracosanoic acid (C24:0)Docosanoic acid (C22:0)DemenciaDémencesAcide tétracosanoique (C24:0)PeroxysomeAcide docosanoIque (C22:0)Alzheimer’s diseaseBiomarkersLipotoxicity
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Membrane topology of gp41 and amyloid precursor protein: Interfering transmembrane interactions as potential targets for HIV and Alzheimer treatment

2009

AbstractThe amyloid precursor protein (APP), that plays a critical role in the development of senile plaques in Alzheimer disease (AD), and the gp41 envelope protein of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome (AIDS), are single-spanning type-1 transmembrane (TM) glycoproteins with the ability to form homo-oligomers. In this review we describe similarities, both in structural terms and sequence determinants of their TM and juxtamembrane regions. The TM domains are essential not only for anchoring the proteins in membranes but also have functional roles. Both TM segments contain GxxxG motifs that drive TM associations within the li…

BiophysicsHIV InfectionsBiologyGp41BiochemistryArticleTransmembrane segmentAmyloid beta-Protein PrecursorMembranes (Biologia)Alzheimer DiseaseAmyloid precursor proteinAnimalsHumansSenile plaqueschemistry.chemical_classificationCell MembraneMembraneHIVCell Biologygp41HIV Envelope Protein gp41Transmembrane proteinVirusCell biologyTransmembrane domainchemistryBiochemistryAmyloid precursor proteinMembrane topologyAlzheimerHIV-1biology.proteinGlycoproteinSequence motifBiochimica et Biophysica Acta (BBA) - Biomembranes
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Amyloid precursor protein in platelets: A peripheral marker for the diagnosis of sporadic AD

2001

BACKGROUND: An altered pattern of amyloid precursor protein (APP) forms consisting in a reduced ratio between the upper (130 kDa) and the lower (106 to 110 kDa) immunoreactivity bands has been described in platelets of patients with AD. OBJECTIVE: To evaluate the sensitivity and the specificity of platelet APP forms' ratio (APPr) as a marker for AD. METHODS: Eighty-five patients with probable AD and 95 control subjects (CON), including healthy individuals and neurologic patients, entered the study. Platelet APPr was evaluated by means of Western Blot analysis and immunostaining in the whole platelet homogenate, and calculated by the ratio between the optical density (OD) of the upper (130 k…

Blood PlateletsMalePathologymedicine.medical_specialtyBlood cellCentral nervous system diseaseAmyloid beta-Protein PrecursorDegenerative diseaseWestern blotAlzheimer DiseasemedicineAmyloid precursor proteinHumansPlateletAgedPsychiatric Status Rating Scalesmedicine.diagnostic_testbiologybusiness.industryMiddle Agedmedicine.diseaseAbnormalities in the pattern of platelet amyloid precursor protein forms in patients with mild cognitive impairment and Alzheimer diseasemedicine.anatomical_structureAmyloid precursor proteinbiology.proteinFemaleSettore MED/26 - NeurologiaNeurology (clinical)Alzheimer's diseasebusinessImmunostainingBiomarkers
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Amyloid precursor protein in platelets of patients with Alzheimer disease: effect of acetylcholinesterase inhibitor treatment.

2001

BACKGROUND:Amyloid precursor protein (APP) forms with apparent molecular weights of 130, 110, and 106 kd are present in human platelets. It has been demonstrated that Alzheimer disease (AD) is specifically associated with a decreased APP forms ratio in platelets. OBJECTIVE:To investigate whether acetylcholinesterase (AChE) inhibitor treatment modifies the ratio of platelet APP forms in patients with AD. PATIENTS AND METHODS:From a large sample of patients with probable AD, 30 with mild to moderate AD were selected. Each patient underwent a clinical evaluation including the Mini-Mental State Examination (MMSE) and platelet APP forms analysis at baseline and after 30 days. During this interva…

Blood PlateletsMalemedicine.medical_specialtyIsoformmedicine.drug_classBlotting WesternAlzheimer disease; biomarker; platelet; Amyloid Precursor Protein; Isoformchemistry.chemical_compoundAmyloid beta-Protein PrecursorArts and Humanities (miscellaneous)PiperidinesDonepezil HydrochlorideInternal medicinemental disordersAmyloid precursor proteinMedicineHumansPlateletDonepezilLongitudinal StudiesDonepezilCholinesteraseAgedamyloid alzheimer diseaseplateletbiologybusiness.industryMiddle AgedAcetylcholinesteraseEndocrinologychemistryAcetylcholinesterase inhibitorEnzyme inhibitorIndansAmyloid Precursor Proteinbiology.proteinbiomarkerSettore MED/26 - NeurologiaFemaleNeurology (clinical)Cholinesterase InhibitorsAlzheimer diseasebusinessmedicine.drugFollow-Up Studies
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Inflammatory Chemokines Expression Variations and Their Receptors in APP/PS1 Mice

2021

Background: In Alzheimer’s disease (AD), an increase in inflammation is distinctive. Amyloid precursor protein plus presenilin-1 (APP/PS1 mice) is a model for this illness. Chemokines secreted by central nervous system (CNS) cells could play multiple important roles in AD. Data looking for the chemokines involved in inflammatory mechanisms are lacking. To understand the changes that occur in the inflammation process in AD, it is necessary to improve strategies to act on specific inflammatory targets. Objective: Chemokines and their receptors involved in phagocytosis, demyelination, chemotaxis, and coagulation were the objective of our study. Methods: Female APPswe/PS1 double-transgenic mice…

CCR1CCR2ChemokineCCR3CCR4Mice TransgenicCCL7Amyloid beta-Protein PrecursorMiceChemokine receptorAlzheimer Diseasemental disordersAnimalsInflammationAmyloid beta-PeptidesbiologyGeneral NeuroscienceBrainChemotaxisGeneral MedicineDisease Models AnimalPsychiatry and Mental healthClinical PsychologyImmunologybiology.proteinFemaleReceptors ChemokineChemokinesGeriatrics and GerontologyJournal of Alzheimer's Disease
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Rebalancing β-Amyloid-Induced Decrease of ATP Level by Amorphous Nano/Micro Polyphosphate: Suppression of the Neurotoxic Effect of Amyloid β-Protein …

2017

Morbus Alzheimer neuropathology is characterized by an impaired energy homeostasis of brain tissue. We present an approach towards a potential therapy of Alzheimer disease based on the high-energy polymer inorganic polyphosphate (polyP), which physiologically occurs both in the extracellular and in the intracellular space. Rat pheochromocytoma (PC) 12 cells, as well as rat primary cortical neurons were exposed to the Alzheimer peptide Aβ25-35. They were incubated in vitro with polyphosphate (polyP); ortho-phosphate was used as a control. The polymer remained as Na+ salt; or complexed in a stoichiometric ratio to Ca2+ (Na-polyP[Ca2+]); or was processed as amorphous Ca-polyP microparticles (C…

Calcium Phosphates0301 basic medicineIntracellular SpacePeptidelcsh:Chemistrychemistry.chemical_compoundAdenosine TriphosphateX-Ray DiffractionPolyphosphatesSpectroscopy Fourier Transform Infraredprimary rat cortex neuronslcsh:QH301-705.5SpectroscopyCerebral CortexNeuronschemistry.chemical_classificationmicroparticlesChemistryβ-amyloidGeneral Medicinepathological conditions signs and symptomsComputer Science Applicationsneurotoxic effectsurgical procedures operativeBiochemistryAlzheimer's diseaseIntracellularCell Survivalβ-amyloid; calcium polyphosphate; microparticles; neurotoxic effect; adenosine triphosphate level; PC12 cells; primary rat cortex neuronsArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineExtracellularotorhinolaryngologic diseasesAnimalsPhysical and Theoretical ChemistryMolecular BiologyneoplasmsAmyloid beta-PeptidesPolyphosphateOrganic ChemistryNeurotoxicityPC12 cellsmedicine.diseaseIn vitrodigestive system diseasesRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999BiophysicsNanoparticlesAdenosine triphosphatecalcium polyphosphateadenosine triphosphate levelInternational Journal of Molecular Sciences
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Building an advocacy model to improve the dementia-capability of health plans in California

2021

Background Given the high and growing prevalence of Alzheimer's disease and related dementias, and the intensity of this population's care needs, it is imperative that healthcare systems increase their capacity to effectively serve people living with dementia (PLwD). The Dementia Cal MediConnect (Dementia CMC) project proposes an advocacy model that may foster dementia-capable systems change. Methods The Dementia CMC project was a 5-year partnership (2013-2018) between local Alzheimer's organizations and 10 managed care health plans (HPs) in California's duals demonstration. It used an advocacy model with the following steps: (1) Identify dementia-capable best practices to set as systems ch…

Capacity BuildingSystems AnalysisReferralBest practicePopulationPatient AdvocacyPublic-Private Sector PartnershipsCaliforniaNursingAlzheimer DiseaseHumansMedicineDementiaBusiness caseeducationeducation.field_of_studyGovernmentbusiness.industrymedicine.diseaseOrganizational InnovationGeneral partnershipVDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Geriatri: 778Managed careDementiasense organsGeriatrics and GerontologybusinessDelivery of Health Care
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Central nicotinic receptors, neurotrophic factors and neuroprotection

2000

The multiple combinations of nAChR subunits identified in central nervous structures possess distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely ind…

Cell SurvivalAgonist-antagonistCentral nervous systemReceptors Nicotiniccomplex mixturesNeuroprotectionBehavioral NeuroscienceNeurotrophic factorsmental disordersmedicineAnimalsHumansNerve Growth FactorsAcetylcholine receptorNeuronsRegulation of gene expressionbiologymusculoskeletal neural and ocular physiologyBrainHaplorhinimedicine.diseaseRatsNeuroprotective Agentsmedicine.anatomical_structurenervous systembiology.proteinFibroblast Growth Factor 2sense organsAlzheimer's diseasePsychologyNeuroscienceNeurotrophinBehavioural Brain Research
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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