0000000000013744

AUTHOR

Giacoma Galizzi

showing 8 related works from this author

Retinal oxidation, apoptosis and age- and sex-differences in the mnd mutant mouse, a model of neuronal ceroid lipofuscinosis

2004

Retinal degeneration is an early and progressive event in many forms of neuronal ceroid lipofuscinoses (NCLs), a heterogeneous group of neurodegenerative disorders with unknown pathogenesis. We here used the mutant motor neuron degeneration (mnd) mouse, a late-infantile NCL variant, to investigate the retinal oxidative state and apoptotic cell death as a function of age and sex. Total superoxide dismutase (SOD) activities and thiobarbituric acid-reactive substance (TBARS) levels revealed progressive increases in retinal oxyradicals and lipid peroxides of mnd mice of both sexes. Female mnd retinas showed a higher oxidation rate and consistently exhibited the 4-hydroxy-2-nonenal (4-HNE)-adduc…

MaleRetinal degenerationPathologymedicine.medical_specialtyApoptosisBiologymedicine.disease_causeThiobarbituric Acid Reactive SubstancesRetinaMiceMice Neurologic Mutantschemistry.chemical_compoundSex FactorsNeuronal Ceroid-LipofuscinosesIn Situ Nick-End LabelingmedicineAnimalsOuter nuclear layerMolecular BiologyAldehydesRetinaTUNEL assayLipid peroxideCaspase 3Superoxide DismutaseGeneral NeuroscienceRetinal DegenerationRetinalmedicine.diseaseImmunohistochemistryEnzyme ActivationMice Inbred C57BLDisease Models AnimalOxidative Stressmedicine.anatomical_structureBiochemistrychemistryCaspasesFemaleNeuronal ceroid lipofuscinosisNeurology (clinical)Oxidation-ReductionOxidative stressDevelopmental BiologyBrain Research
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Altered insulin pathway compromises mitochondrial function and quality control both in in vitro and in vivo model systems.

2021

Abstract Altered insulin signaling and insulin resistance are considered the link between Alzheimer's disease (AD) and metabolic syndrome. Here, by using an in vitro and an in vivo model, we investigated the relationship between these disorders focusing on neuronal mitochondrial dysfunction and mitophagy. In vitro Aβ insult induced the opening of mitochondrial permeability transition pore (mPTP), mitochondrial membrane potential (ΔΨm) loss, and apoptosis while insulin addition ameliorated these dysfunctions. The same alterations were detected in a 16 weeks of age mouse model of diet-induced obesity and insulin resistance. In addition, we detected an increase of fission related proteins and …

MaleAgingAmyloid beta-Peptidemedicine.medical_treatmentMetabolic diseasePINK1Insulin pathway Neurodegeneration Metabolic diseases Mitochondrion Mitophagy AgingMitochondrionDiet High-FatParkinNOMiceInsulin resistanceMetabolic DiseasesCell Line TumorMitophagymedicineAnimalsHumansInsulinMitochondrionNeurodegenerationMolecular BiologyAmyloid beta-PeptidesbiologyAnimalChemistryInsulinMitophagyCell Biologymedicine.diseaseCell biologyMitochondriaMice Inbred C57BLInsulin receptorMitochondrial permeability transition porebiology.proteinMolecular MedicineInsulin ResistanceInsulin pathwayHumanSignal TransductionMitochondrion
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A Natural Dietary Supplement with a Combination of Nutrients Prevents Neurodegeneration Induced by a High Fat Diet in Mice

2018

Obesity and metabolic disorders can be risk factors for the onset and development of neurodegenerative diseases. The aim of the present study was to investigate the protective effects of a natural dietary supplement (NDS), containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin, on dysmetabolism and neurodegeneration in the brains of high fat diet (HFD)-fed mice. Decrease in the expression of FACL-4, CerS-1, CerS-4, cholesterol concentration and increase in the insulin receptor expression and insulin signaling activation, were found in brains of NDS-treated HFD brains in comparison with HFD untreated-mice, suggesting that NDS is able to prevent brain lipid accumulation and …

Male0301 basic medicineobesityAntioxidantmedicine.medical_treatmentAnti-Inflammatory AgentsApoptosismedicine.disease_causeSettore BIO/09 - FisiologiaAntioxidantsLipid peroxidationchemistry.chemical_compound0302 clinical medicineinsulin resistanceInsulinnatural antioxidantsNutrition and DieteticsbiologyChemistryneurodegenerationobesity; HFD mice; natural antioxidants; insulin resistance; neurodegenerationBrainfood and beveragesNeurodegenerative Diseaseslipids (amino acids peptides and proteins)Inflammation Mediatorsmedicine.symptomlcsh:Nutrition. Foods and food supplySignal Transductionmedicine.medical_specialtylcsh:TX341-641endocrinology_metabolomicsInflammationDiet High-FatNeuroprotectionArticle03 medical and health sciencesInsulin resistanceInternal medicinemedicineAnimalsHFD miceCholesterolInsulinLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressInsulin receptor030104 developmental biologyEndocrinologyDietary SupplementsNerve Degenerationbiology.proteinLipid Peroxidationnatural antioxidant030217 neurology & neurosurgeryOxidative stressFood ScienceNutrients
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Regular Intake of Pistachio Mitigates the Deleterious Effects of a High Fat-Diet in the Brain of Obese Mice

2020

Obesity has been associated with neurodegeneration and cognitive dysfunctions. Recent data showed that pistachio consumption is able to prevent and ameliorate dyslipidemia, hepatic steatosis, systemic and adipose tissue inflammation in mice fed a high-fat diet (HFD). The present study investigated the neuroprotective effects of pistachio intake in HFD mice. Three groups of mice were fed a standard diet (STD), HFD, or HFD supplemented with pistachio (HFD-P) for 16 weeks. Metabolic parameters (oxidative stress, apoptosis, and mitochondrial dysfunction) were analyzed by using specific assays and biomarkers. The pistachio diet significantly reduced the serum levels of triglycerides and choleste…

0301 basic medicinemedicine.medical_specialtyobesityPhysiologyClinical BiochemistryAdipose tissuepistachiomedicine.disease_causeBiochemistryArticleSuperoxide dismutase03 medical and health sciences0302 clinical medicineInsulin resistanceInternal medicinemedicineoxidative stressMolecular Biologychemistry.chemical_classificationReactive oxygen speciesoxidative strebiologybusiness.industrylcsh:RM1-950digestive oral and skin physiologyneurodegenerationfood and beveragesnutritional and metabolic diseasesCell Biologymedicine.diseaseHeme oxygenaselcsh:Therapeutics. Pharmacology030104 developmental biologyEndocrinologychemistrybiology.proteinlipids (amino acids peptides and proteins)HFDSteatosisbusiness030217 neurology & neurosurgeryDyslipidemiaOxidative stresshormones hormone substitutes and hormone antagonists
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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
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Synaptosomes: new vesicles for neuronal mitochondrial transplantation

2021

Abstract Background Mitochondrial dysfunction is a critical factor in the onset and progression of neurodegenerative diseases. Recently, mitochondrial transplantation has been advised as an innovative and attractive strategy to transfer and replace damaged mitochondria. Here we propose, for the first time, to use rat brain extracted synaptosomes, a subcellular fraction of isolated synaptic terminal that contains mitochondria, as mitochondrial delivery systems. Results Synaptosome preparation was validated by the presence of Synaptophysin and PSD95. Synaptosomes were characterized in terms of dimension, zeta potential, polydispersity index and number of particles/ml. Nile Red or CTX-FITCH la…

MaleFIS1Mitochondrial DNAlcsh:Medical technologylcsh:BiotechnologyBiomedical EngineeringPharmaceutical ScienceMedicine (miscellaneous)BioengineeringMitochondrionDNA MitochondrialApplied Microbiology and BiotechnologyMembrane Potentials03 medical and health sciencesDrug Delivery Systems0302 clinical medicinelcsh:TP248.13-248.65medicineAnimalsHomeostasisProtein Interaction Domains and MotifsNeurodegenerationDelivery system030304 developmental biologyMitochondrial transplantationSynaptosome0303 health sciencesbiologyChemistryResearchCytochrome cNeurodegenerationSynaptosomes Mitochondria Neurodegeneration Delivery system Mitochondrial transplantationCytochromes cmedicine.diseaseRatsCell biologyMitochondriaTransplantationlcsh:R855-855.5Cytoplasmbiology.proteinMolecular Medicine030217 neurology & neurosurgerySubcellular FractionsSynaptosomes
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Expression of vesicle-associated membrane-protein-associated protein B cleavage products in peripheral blood leukocytes and cerebrospinal fluid of pa…

2013

Background and purpose Vesicle-associated membrane-protein-associated protein B (VAPB) is an endoplasmic reticulum (ER) resident protein participating in ER function, vesicle trafficking, calcium homeostasis and lipid transport. Its N-terminal domain, named MSP, is cleaved and secreted, serving as an extracellular ligand. VAPB mutations are linked to autosomal-dominant motor neuron diseases, including amyotrophic lateral sclerosis (ALS) type 8. An altered VAPB function is also suspected in sporadic ALS (SALS). Methods The expression pattern of VAPB cleavage and secreted products in the peripheral blood leukocytes (PBL) and cerebrospinal fluid (CSF) of SALS patients and neurological controls…

MalePathologymedicine.medical_specialtyamyotrophic lateral sclerosisnematode major sperm proteinproteolysisVesicular Transport ProteinsStatistics Nonparametriccerebrospinal fluidCerebrospinal fluidparasitic diseasesLeukocytesmedicineHumansperipheral blood leukocytesSecretionAmyotrophic lateral sclerosisAgedbiologybusiness.industryEndoplasmic reticulumvesicle-associated membrane-protein-associated protein AMiddle AgedVAPBmedicine.diseaseMolecular biologyvesicle-associated membrane-protein-associated protein Bamyotrophic lateral sclerosis cerebrospinal fluid nematode major sperm protein peripheral blood leukocytes proteolysis vesicleassociated membraneprotein- associated protein A vesicleassociated membraneprotein- associated protein BMolecular WeightBlotSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaVesicle-associated membrane proteinNeurologyMutationbiology.proteinSettore MED/26 - NeurologiaFemaleNeurology (clinical)Antibodybusiness
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Additional file 1 of Synaptosomes: new vesicles for neuronal mitochondrial transplantation

2021

Additional file 1: Figure S1. A) Morphological analysis of LAN5 cells incubated with different doses (5-10 and 20 µl, which correspond to concentration of 2.5 × 107; 5.1 × 107; 10.2 × 107 particles/100µl respectively) of synaptosomes (Synap). B) Nuclear staining by fluorescence probe Hoechst 3341 of LAN5 cells incubated with different doses (5-10 and 20 µl) of synaptosomes (Synap).

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