Search results for "Amy"

showing 10 items of 1486 documents

An update on intracerebral stem cell grafts.

2018

Introduction: Primary neurological disorders are notoriously debilitating and deadly, and over the past four decades stem cell therapy has emerged as a promising treatment. Translation of stem cell therapies from the bench to the clinic requires a better understanding of delivery protocols, safety profile, and efficacy in each disease. Areas covered: In this review, benefits and risks of intracerebral stem cell transplantation are presented for consideration. Milestone discoveries in stem cell applications are reviewed to examine the efficacy and safety of intracerebral stem cell transplant therapy for disorders of the central nervous system and inform design of translatable protocols for c…

0301 basic medicineOncologymedicine.medical_specialtyParkinson's diseaseTraumatic brain injurymedicine.medical_treatmentmulti-system atrophyNeuroprotection03 medical and health sciencesGraft vs Host Reaction0302 clinical medicineHuntington's diseaseCentral Nervous System DiseasesRisk FactorsInternal medicineMedicineAnimalsHumansPharmacology (medical)amyotrophic lateral sclerosiAmyotrophic lateral sclerosisStem cellbusiness.industryGeneral NeuroscienceMultiple sclerosistraumatic brain injuryStem-cell therapymedicine.diseasestroke030104 developmental biologyBlood-Brain Barriermultiple sclerosiParkinson’s diseaseneuroprotectionNeurology (clinical)Stem cellbusiness030217 neurology & neurosurgeryHuntington’s diseaseStem Cell TransplantationExpert review of neurotherapeutics
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Vitamin D and Its Analogues Decrease Amyloid-β (Aβ) Formation and Increase Aβ-Degradation

2017

Alzheimer’s disease (AD) is characterized by extracellular plaques in the brain, mainly consisting of amyloid-β (Aβ), as derived from sequential cleavage of the amyloid precursor protein. Epidemiological studies suggest a tight link between hypovitaminosis of the secosteroid vitamin D and AD. Besides decreased vitamin D level in AD patients, an effect of vitamin D on Aβ-homeostasis is discussed. However, the exact underlying mechanisms remain to be elucidated and nothing is known about the potential effect of vitamin D analogues. Here we systematically investigate the effect of vitamin D and therapeutically used analogues (maxacalcitol, calcipotriol, alfacalcidol, paricalcitol, doxercalcife…

0301 basic medicineParicalcitolPlaque Amyloidvitamin Damyloid precursor proteinlcsh:ChemistrySecosteroidMicechemistry.chemical_compound0302 clinical medicinevitamin D analoguesvitamin D; vitamin D analogues; amyloid precursor protein; amyloid-β; secretases; Aβ-degradationAmyloid precursor proteinlcsh:QH301-705.5CalcipotriolSpectroscopybiologysecretasesBrainAlfacalcidolVitaminsGeneral Medicine3. Good healthComputer Science ApplicationsFemalemedicine.drugmedicine.medical_specialtyAβ-degradationNicastrinamyloid-βArticleCatalysisInorganic Chemistry03 medical and health sciencesCell Line TumorInternal medicinemedicineVitamin D and neurologyAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyAmyloid beta-PeptidesOrganic ChemistryMice Inbred C57BL030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999chemistryProteolysisbiology.proteinAmyloid Precursor Protein SecretasesAmyloid precursor protein secretase030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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A longitudinal DTI and histological study of the spinal cord reveals early pathological alterations in G93A-SOD1 mouse model of amyotrophic lateral s…

2017

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective motor neuron degeneration in the motor cortex, brainstem and spinal cord. It is generally accepted that ALS is caused by death of motor neurons, however the exact temporal cascade of degenerative processes is not yet completely known. To identify the early pathological changes in spinal cord of G93A-SOD1 AIS mice we performed a comprehensive longitudinal analysis employing diffusion-tensor magnetic resonance imaging alongside histology and electron microscopy, in parallel with peripheral nerve histology. We showed the gradient of degeneration appearance in spinal cord white and gray matter, startin…

0301 basic medicinePathologyNeurologyTime FactorsMotor neuron diseasesSensory Receptor CellMice0302 clinical medicineImage Processing Computer-AssistedAxonAmyotrophic lateral sclerosisGray MatterAnthracenesWhite MatterMitochondriamedicine.anatomical_structureDiffusion Tensor ImagingNeurologySpinal CordG93A-SOD1 miceBrainstemHumanMotor cortexmedicine.medical_specialtyAxon degenerationTime FactorSensory Receptor CellsSOD1Mice TransgenicWhite matter03 medical and health sciencesMagnetic resonance imagingDevelopmental NeuroscienceMicroscopy Electron TransmissionmedicineElectron microscopyAnimalsHumansMotor neuron diseaseAmyotrophic lateral sclerosiAnimalbusiness.industrySuperoxide DismutaseAmyotrophic Lateral SclerosisSpinal cordmedicine.diseaseAmyotrophic lateral sclerosisMice Inbred C57BLDisease Models Animal030104 developmental biologyAnthracenebusinessNeuroscience030217 neurology & neurosurgeryExperimental neurology
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Mice are not Men: ADAM30 Findings Emphasize a Broader Look Towards Murine Alzheimer's Disease Models

2016

Due to the growing population of people at advanced age, the number of patients affected by Alzheimer's disease (AD) is increasing tremendously. In 2015 about 46.8 million people suffered from AD worldwide which is estimated to increase to 131.5 million by 2050. Brains of AD patients all show a common histopathology; they are marked by an atrophy and degeneration that is caused by a severe loss of neurons and synapses (Braak and Del Tredici, 2012). Moreover, so-called extracellular senile plaques that consist of predominantly amyloid β (Aβ) peptides can be detected in the grey matter where they surround neurons. Since generation of Aβ peptides is hypothesized to play a major role in AD path…

0301 basic medicinePathologymedicine.medical_specialtyADAM10Populationlcsh:MedicineMice TransgenicGrey matterBiologyGeneral Biochemistry Genetics and Molecular BiologyPathogenesisMice03 medical and health sciences0302 clinical medicineAtrophyAlzheimer DiseasemedicineAmyloid precursor proteinAnimalsHumansSenile plaqueseducationlcsh:R5-920education.field_of_studylcsh:RP3 peptideGeneral Medicinemedicine.diseaseADAM ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureDisease ProgressionCommentarybiology.proteinlcsh:Medicine (General)Neuroscience030217 neurology & neurosurgeryEBioMedicine
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Amyotrophic Lateral Sclerosis, a Multisystem Pathology: Insights into the Role of TNFα

2017

Amyotrophic lateral sclerosis (ALS) is considered a multifactorial, multisystem disease in which inflammation and the immune system play important roles in development and progression. The pleiotropic cytokine TNFαis one of the major players governing the inflammation in the central nervous system and peripheral districts such as the neuromuscular and immune system. Changes in TNFαlevels are reported in blood, cerebrospinal fluid, and nerve tissues of ALS patients and animal models. However, whether they play a detrimental or protective role on the disease progression is still not clear. Our group and others have recently reported opposite involvements of TNFR1 and TNFR2 in motor neuron dea…

0301 basic medicinePathologymedicine.medical_specialtyAmyotrophic Lateral Sclerosis; Animals; Humans; Motor Neurons; T-Lymphocytes Regulatory; Tumor Necrosis Factor-alphamedicine.medical_treatmentT-LymphocytesCentral nervous systemImmunologyAmyotrophic lateral sclerosis inflammation TNFαInflammationReview ArticleT-Lymphocytes Regulatory03 medical and health sciences0302 clinical medicineImmune systemCerebrospinal fluidImmunology; Cell BiologyTNFαlcsh:PathologyMedicineAnimalsHumansAmyotrophic lateral sclerosisMotor Neuronsbusiness.industryTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisCell BiologyMotor neuronmedicine.diseaseRegulatory3. Good health030104 developmental biologymedicine.anatomical_structureCytokineinflammationImmunologyTumor necrosis factor alphamedicine.symptombusiness030217 neurology & neurosurgerylcsh:RB1-214
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Subchronic administration of auranofin reduced amyloid-β plaque pathology in a transgenic APPNL-G-F/NL-G-F mouse model

2020

Abstract Alzheimer’s disease (AD) is the most common cause of dementia. Neuropathological processes, including the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles, and neuroinflammation, lead to cognitive impairment at middle and eventually later stages of AD progression. Over the last decade, focused efforts have explored repurposed drug approaches for AD pathophysiological mechanisms. Recently, auranofin, an anti-inflammatory drug, was shown to have therapeutic potential in a number of diseases in addition to rheumatoid arthritis. Surprisingly, no data regarding the effects of auranofin on cognitive deficits in AD mice or the influence of auranofin on Aβ pathology and n…

0301 basic medicinePathologymedicine.medical_specialtyAuranofinGlial fibrillary acidic proteinbiologybusiness.industryAmyloid betaGeneral NeuroscienceGlutamate decarboxylaseHippocampusPathophysiology03 medical and health sciences030104 developmental biology0302 clinical medicineSynaptic plasticitybiology.proteinMedicineNeurology (clinical)businessMolecular Biology030217 neurology & neurosurgeryNeuroinflammationDevelopmental Biologymedicine.drugBrain Research
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Acute onset of bulbar amyotrophic lateral sclerosis after flu – look at the differential diagnosis: A case report

2018

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting upper and lower motor neurones. It can be either familial (fALS) or sporadic (sALS). ALS is characterized by muscle weakness and atrophy that can involve the limbs and trunk (i.e. the spinal form of the disease) or speech and swallowing (i.e. the bulbar form). The aetiology of sALS remains unclear although a gene–environment interaction has been proposed as a concomitant trigger for the neurodegenerative process together with viral infections, smoking, heavy metals and pesticide exposure. Herein, we report the case of a 67-year-old woman who experienced an acute onset of bulbar ALS with an atypical clinical cours…

0301 basic medicinePathologymedicine.medical_specialtyMedicine (General)DiseaseCase Reportsacute onsetBiochemistryDiagnosis Differential03 medical and health sciences0302 clinical medicineAtrophyR5-920Swallowingsporadic amyotrophic lateral sclerosisDiagnosisdifferential diagnosisInfluenza HumanMedicineHumansAmyotrophic lateral sclerosisAgedbulbar amyotrophic lateral sclerosisbusiness.industryBiochemistry (medical)Amyotrophic Lateral SclerosisMuscle weaknessCell BiologyGeneral Medicinemedicine.diseaseTrunkInfluenza030104 developmental biologyDifferentialAcute DiseaseEtiologyFamilial amyotrophic lateral sclerosisFemaleacute onset; bulbar amyotrophic lateral sclerosis; differential diagnosis; Familial amyotrophic lateral sclerosis; sporadic amyotrophic lateral sclerosis; Acute Disease; Aged; Amyotrophic Lateral Sclerosis; Diagnosis Differential; Female; Humans; Influenza HumanDifferential diagnosismedicine.symptombusiness030217 neurology & neurosurgeryHumanJournal of International Medical Research
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Nutritional Wheat Amylase-Trypsin Inhibitors Promote Intestinal Inflammation via Activation of Myeloid Cells.

2016

Background & Aims Wheat amylase-trypsin inhibitors (ATIs) are nutritional activators of innate immunity, via activation of the toll-like receptor 4 (TLR4) on myeloid cells. We aimed to characterize the biologic activity of ATIs in various foods and their effect on intestinal inflammation. Methods We selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat, rye, barley, quinoa, amaranth, soya, lentils, and rice) or processed (such as pizza, pasta, bread, and biscuits). ATIs were extracted and their biological activities determined in TLR4-responsive mouse and human cell lines. Effects of oral ATIs on intestinal inflammation were determined in health…

0301 basic medicinePharmacologyAdaptive Immunitychemistry.chemical_compoundMice0302 clinical medicineMesenteric lymph nodesMesenteryMyeloid CellsTriticumPlant ProteinsToll-like receptorDextran SulfateGastroenterologyfood and beveragesColitisIntestinesmedicine.anatomical_structureAmylases030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsInterferon InducersGlutensColonDuodenumInflammationIleumBiologyCell Line03 medical and health sciencesDiet Gluten-FreeIleummedicineAnimalsHumansColitisInflammationInnate immune systemHepatologymedicine.diseaseImmunity InnateMice Inbred C57BLToll-Like Receptor 4Celiac Disease030104 developmental biologyPoly I-CchemistryPolyinosinic:polycytidylic acidImmunologyLymph NodesWheat allergyGastroenterology
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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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Identification of Phlogacantholide C as a Novel ADAM10 Enhancer from Traditional Chinese Medicinal Plants

2016

Background: Alzheimer’s disease is one of the most prevalent dementias in the elderly population with increasing numbers of patients. One pivotal hallmark of this disorder is the deposition of protein aggregates stemming from neurotoxic amyloid-beta peptides. Synthesis of those peptides has been efficiently prevented in AD model mice by activation of an enzyme called alpha-secretase. Therefore, drugs with the capability to increase the expression of this enzyme, named ADAM10, have been suggested as a valuable therapeutic medication. Methods: We investigated 69 substances from a drug library derived from traditional Chinese medicine by luciferase reporter assay in human neuronal cells for th…

0301 basic medicinePhlogacanthus curviflorusADAM10lcsh:MedicineProtein aggregationBiologyPharmacologyArticle03 medical and health sciences0302 clinical medicineWestern blotGene expressionPhlogacantholide CmedicineAmyloid precursor proteinSecretionEnhancerADAM10; Amyloid precursor protein; Alzheimer’s disease; Norkurarinol; Phlogacantholide C; <i>Phlogacanthus curviflorus</i>; <i>Sophora flavescens</i>chemistry.chemical_classificationmedicine.diagnostic_testlcsh:RADAM10Norkurarinol030104 developmental biologyEnzymechemistrySophora flavescensAmyloid precursor proteinbiology.proteinAlzheimer’s disease030217 neurology & neurosurgeryMedicines
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