Search results for "alzheimer disease"

showing 10 items of 428 documents

Obstructive sleep apnea and Alzheimer’s disease-related cerebrospinal fluid biomarkers in mild cognitive impairment

2020

Abstract Previous studies have demonstrated that sleep-breathing disorders, and especially obstructive sleep apnea (OSA), can be observed in patients with a higher risk of progression to Alzheimer’s disease (AD). Recent evidence indicates that cerebrospinal fluid (CSF) AD-biomarkers are associated with OSA. In this study, we investigated these associations in a sample of patients with mild cognitive impairment (MCI), a condition that is considered the first clinical phase of AD, when patients showed biomarkers consistent with AD pathology. A total of 57 patients (mean age = 66.19; SD = 7.13) with MCI were included in the study. An overnight polysomnography recording was used to assess objec…

medicine.medical_specialtyHeart diseaseRapid eye movement sleeptau ProteinsPolysomnography03 medical and health sciences0302 clinical medicineAlzheimer DiseasePhysiology (medical)Internal medicinemedicineHumansCognitive DysfunctionAgedSleep Apnea ObstructiveAmyloid beta-Peptidesmedicine.diagnostic_testbusiness.industryApneamedicine.diseaseSleep in non-human animalsPeptide FragmentsObstructive sleep apnea030228 respiratory systemCardiologyNeurology (clinical)medicine.symptombusinessHypopneaBody mass indexBiomarkers030217 neurology & neurosurgerySleep
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Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer's disease.

2017

Alzheimer's disease (AD) is the most prevalent form of dementia. The exact pathophysiology of this disease remains incompletely understood and safe and effective therapies are required. AD is highly correlated with neuroinflammation and oxidative stress in brain causing neuronal loss. Nuclear factor of activated B-cells (NF-κB) is involved in physiological inflammatory processes and thus representing a promising target for inflammation-based AD therapy. Phytochemicals are able to interfere with the NF-κB pathway. They inhibit the phosphorylation or the ubiquitination of signaling molecules, and thus, inhibit the degradation of IκB. The translocation of NF-κB to the nucleus and subsequent tr…

0301 basic medicinePterostilbenePhytochemicalsResveratrolPharmacologymedicine.disease_cause03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAlkaloidsAlzheimer DiseasemedicineAnimalsHumansPharmacologyNF-kappa BPolyphenolsNF-κBVitaminsTetrandrine030104 developmental biologychemistryCurcuminObovatol030217 neurology & neurosurgeryOxidative stressAnatabinePharmacological research
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An intraoral drug delivery device for long term therapies: application in Alzheimer’s disease

2009

IntelliDrug intraoral device Alzheimer diseaseSettore CHIM/09 - Farmaceutico Tecnologico Applicativo
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Amyloid in Alzheimer’s Disease: Guilty Beyond Reasonable Doubt?

2017

Recently failed antiamyloidogenic trials call for an objective reassessment of the dominating amyloid cascade hypothesis of Alzheimer's disease (AD). Ongoing efforts focusing on amyloid β protein (Aβ), its deposition, and its removal need to be complemented by more intensive research in new directions. Those may either integrate amyloid pathology or will propose pathogenetic routes independent of Aβ in the search for the causes of AD.

0301 basic medicinePharmacologyAmyloidReasonable doubtAmyloid pathologyAmyloidAmyloid βDiseaseToxicology03 medical and health sciences030104 developmental biology0302 clinical medicineAlzheimer DiseaseAnimalsHumansAmyloid cascadePsychologyNeuroscience030217 neurology & neurosurgeryTrends in Pharmacological Sciences
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ADAM10 in Alzheimer's disease: Pharmacological modulation by natural compounds and its role as a peripheral marker.

2019

Abstract Alzheimer’s disease (AD) represents a global burden in the economics of healthcare systems. Amyloid-β (Aβ) peptides are formed by amyloid-β precursor protein (AβPP) cleavage, which can be processed by two pathways. The cleavage by the α-secretase A Disintegrin And Metalloprotease 10 (ADAM10) releases the soluble portion (sAβPPα) and prevents senile plaques. This pathway remains largely unknown and ignored, mainly regarding pharmacological approaches that may act via different signaling cascades and thus stimulate non-amyloidogenic cleavage through ADAM10. This review emphasizes the effects of natural compounds on ADAM10 modulation, which eventuates in a neuroprotective mechanism. M…

0301 basic medicineFarmacologiaADAM10DiseaseRM1-950Natural compoundsCleavage (embryo)NeuroprotectionCatechin03 medical and health sciencesADAM10 ProteinAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseDisintegrinHumansSenile plaquesPharmacological modulationPharmacologyMetalloproteinaseAmyloid beta-PeptidesbiologyChemistryPlant ExtractsADAM10ProteinsGinkgo bilobaMembrane ProteinsGeneral Medicineα-SecretaseAlzheimer's disease030104 developmental biologyMalaltia d'AlzheimerNeuroprotective Agents030220 oncology & carcinogenesisPharmaceuticalbiology.proteinTherapeutics. PharmacologyAmyloid Precursor Protein SecretasesNeuroscienceAlzheimer’s diseaseProteïnesBiomarkersBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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From obesity to Alzheimer's disease through insulin resistance

2021

Alzheimer's disease is one of the most frequent forms of dementia. It is a progressive neurodegenerative disease, characterized by presence of amyloid plaques and neurofibrillary tangles in the brain. Obesity is regarded as abnormal fat accumulation with deleterious impact on human health. There is full scientific evidence that obesity and the metabolic comorbidities (e.g., insulin resistance, hyperglycaemia, and type 2 diabetes) are related to Alzheimer's disease and likely in the causative pathway. Numerous studies have identified several overlapping neurodegenerative mechanisms, including oxidative stress, mitochondrial dysfunction, and inflammation. In this review, we present how obesit…

medicine.medical_specialtyEndocrinology Diabetes and MetabolismType 2 diabetesmedicine.disease_causeEndocrinologyInsulin resistanceDownregulation and upregulationAlzheimer DiseaseInternal medicineDiabetes mellitusInternal MedicinemedicineHumansDementiaObesityNeurodegenerationInflammationbusiness.industryNeurodegenerationBrainInsulin resistanceAlzheimer's diseasemedicine.diseaseEndocrinologyDiabetes Mellitus Type 2LipotoxicitybusinessOxidative stressJournal of Diabetes and its Complications
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Why Women Have More Alzheimer's Disease Than Men: Gender and Mitochondrial Toxicity of Amyloid-β Peptide

2010

The main risk factors for developing Alzheimer's disease (AD) are age and gender. The incidence of the disease is higher in women than in men, and this cannot simply be attributed to the higher longevity of women versus men. Thus, there must be a specific pathogenic mechanism to explain the higher incidence of AD cases in women. In this regard, it is notable that mitochondria from young females are protected against amyloid-beta toxicity, generate less reactive oxygen species, and release less apoptogenic signals than those from males. However, all this advantage is lost in mitochondria from old females. Since estrogenic compounds protect against mitochondrial toxicity of amyloid-beta, estr…

MalePhysiologyDiseaseMitochondrionPharmacologyModels BiologicalAlzheimer DiseaseRisk FactorsmedicineHumansSex CharacteristicsAmyloid beta-PeptidesbiologyGinkgo bilobaGeneral NeuroscienceIncidence (epidemiology)EstrogensGeneral Medicinebiology.organism_classificationmedicine.diseaseMitochondriaUp-RegulationClinical trialPsychiatry and Mental healthClinical PsychologyMitochondrial toxicityToxicityFemaleGeriatrics and GerontologySex characteristicsJournal of Alzheimer's Disease
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Genetic risk profiles for Alzheimer's disease: Integration of APOE genotype and variants that up-regulate inflammation

2007

BACKGROUND: A number of studies associate Alzheimer's disease with APOE polymorphism and alleles which favor the increased expression of immunological mediators such as cytokines or acute phase proteins. We integrated this information to better define risk and determine the relative importance of APOE and immunological mediators. METHODS: We investigated functional gene variants for APOE, IL-10 (3 loci), ACT (2 loci), HMGCR, IL-1alpha, IL-1beta, TNF-alpha, IFN-gamma, and IL-6 found for 260 AD patients and 190 controls enrolled in Northern Italy. A fuzzy latent classification approach, namely grade-of-membership analysis (GoM), was taken to identify extreme pure type risk sets, or profiles. …

MaleApolipoprotein EAgingGenotypeDiseaseBiologyApolipoproteins EAlzheimer DiseaseRisk FactorsGenotypeHumansGenetic Predisposition to DiseaseCognitive declineAlleleGeneAgedAged 80 and overGeneticsPolymorphism GeneticGeneral NeuroscienceAge FactorsAcute-phase proteinGenetic VariationAPOE IL-10 ACT HMGCR IL-1alpha IL-1beta TNF-alpha IFN-gamma IL-6 SNPs Grade of memebership Genetic risk profile Alzheimer's diseaseMiddle AgedUp-RegulationFemaleNeurology (clinical)Gene polymorphismInflammation MediatorsGeriatrics and GerontologyDevelopmental Biology
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Very low doses of muscimol and baclofen ameliorate cognitive deficits and regulate protein expression in the brain of a rat model of streptozocin-ind…

2018

Recent studies devoted to neuroprotection have focused on the role of the gamma-aminobutyric acid (GABA) system in regulating neuroinflammatory processes which play a key role in the neurodegenerative processes observed in Alzheimer's disease (AD) by inducing glial cell overactivation and impairing neurotransmission. Data on the efficacy of classical GABA-A and GABA-B receptor agonists (muscimol and baclofen, respectively) in animal models of AD are not available. Moreover, no published studies have examined the ability of optimal doses of these compounds to prevent neuroinflammation, the alterations in neurotransmission and cognitive deficits. In the present study, we used a non-transgenic…

0301 basic medicineMaleBaclofenGlutamate decarboxylaseSpatial LearningPharmacologyNeuroprotectionStreptozocin03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCognitionGABA receptorSTZAlzheimer DiseaseMemoryGlial Fibrillary Acidic ProteinLearningAnimalsRats WistarNeuroinflammationPharmacologyGlial fibrillary acidic proteinbiologyDose-Response Relationship DrugChemistryGABAA receptorMuscimolBrainRatsDisease Models Animal030104 developmental biologyBaclofennervous systemMuscimolGene Expression RegulationRat model of ADbiology.protein:MEDICINE::Physiology and pharmacology::Pharmacological research [Research Subject Categories]Neuroscience030217 neurology & neurosurgeryEuropean journal of pharmacology
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Choice of reference area in studies of Alzheimer's disease using positron emission tomography with fluorodeoxyglucose-F18

2007

At present, there is still no consensus on the choice of the reference area in positron emission tomography (PET) studies of Alzheimer's disease (AD). In this study, PET scans with fluorodeoxyglucose-F18 were carried out in the following groups of subjects: 47 patients with probable AD, 8 patients with mild cognitive impairment, and 15 age-similar healthy subjects. Scans normalized to the cerebral global mean (CGM), cerebellum (CBL), and the primary sensorimotor cortex (SMC). We evaluated the effect of the different count normalization procedures on the accuracy of (18)F-FDG PET to detect AD-specific metabolic abnormalities (voxel-based group comparison) and to differentiate between patient…

MaleNormalization (statistics)Pathologymedicine.medical_specialtyAdolescentNeuroscience (miscellaneous)Neuropsychological TestsStatistical parametric mappingGyrus CinguliSeverity of Illness IndexCentral nervous system diseaseAlzheimer DiseaseFluorodeoxyglucose F18CerebellumParietal LobemedicineHumansDementiaRadiology Nuclear Medicine and imagingAgedFluorodeoxyglucosemedicine.diagnostic_testbusiness.industryCognitive disorderMotor CortexSomatosensory Cortexmedicine.diseaseTemporal LobeFrontal LobePsychiatry and Mental healthPositron emission tomographyPositron-Emission TomographyFemaleRadiopharmaceuticalsAlzheimer's diseaseCognition DisordersNuclear medicinebusinessPsychologymedicine.drugPsychiatry Research: Neuroimaging
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