Search results for "Neuronal degeneration"

showing 4 items of 4 documents

3-Acetylpyridine-induced degeneration and regeneration in the adult lizard brain: a qualitative and quantitative analysis

1997

Abstract The neurotoxin 3-acetylpyridine (3AP) produces highly selective neuronal damage in specific areas of the lizard brain. Following 3AP intoxication, proliferation and migration of replacement neurons born in the ventricular walls lead to regeneration of the lesioned areas. Earlier studies established the time course of 3AP-induced degeneration and subsequent regeneration in the medial cerebral cortex of adult lizards (Font, E., Garcia-Verdugo, J.M., Alcantara, S. and Lopez-Garcia, C., Neuron regeneration reverses 3-acetylpyridine-induced cell loss in the cerebral cortex of adult lizards, Brain Res. , 551 (1991) 230–235 [13] ). Complementary to our previous studies, we now provide a q…

MalePathologymedicine.medical_specialtyDendritic spinePyridinesNeurotoxinsBiologyTransneuronal degenerationsymbols.namesakeCortex (anatomy)medicineAnimalsMolecular BiologyCell NucleusCerebral CortexNeuronsCerebrumGeneral NeuroscienceNeurogenesisBrainLizardsDNAAnatomyNerve Regenerationmedicine.anatomical_structureCerebral cortexNerve DegenerationNissl bodysymbolsFemaleNeurology (clinical)NeuronThymidineDevelopmental BiologyBrain Research
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A comparative evaluation of NB30, NB54 and PTC124 in translational read-through efficacy for treatment of an USH1C nonsense mutation

2012

Translational read-through-inducing drugs (TRIDs) promote read-through of nonsense mutations, placing them in the spotlight of current gene-based therapeutic research. Here, we compare for the first time the relative efficacies of new-generation aminoglycosides NB30, NB54 and the chemical compound PTC124 on retinal toxicity and read-through efficacy of a nonsense mutation in the USH1C gene, which encodes the scaffold protein harmonin. This mutation causes the human Usher syndrome, the most common form of inherited deaf-blindness. We quantify read-through efficacy of the TRIDs in cell culture and show the restoration of harmonin function. We do not observe significant differences in the read…

MaleRetinal DisorderUsher syndromemedia_common.quotation_subjectNonsenseNonsense mutationPeptide Chain Elongation TranslationalCell Cycle ProteinsIn Vitro TechniquesBiologyPharmacologymedicine.disease_causeRetinaCell LineMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRetinal DiseasesIn vivoretinitis pigmentosaRetinitis pigmentosaotorhinolaryngologic diseasesmedicineAnimalsHumansResearch ArticlesAdaptor Proteins Signal Transducingpharmacogenetics030304 developmental biologymedia_commonOxadiazoles0303 health sciencesMutationsensoneuronal degenerationRetinalmedicine.diseasedrug therapy3. Good healthMice Inbred C57BLCytoskeletal ProteinsAminoglycosideschemistryCodon NonsenseMolecular MedicineFemaleUsher syndrome030217 neurology & neurosurgeryEMBO Molecular Medicine
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Direct interaction of the Usher syndrome 1G protein SANS and myomegalin in the retina

2011

Contains fulltext : 96822.pdf (Publisher’s version ) (Closed access) The human Usher syndrome (USH) is the most frequent cause of combined hereditary deaf-blindness. USH is genetically heterogeneous with at least 11 chromosomal loci assigned to 3 clinical types, USH1-3. We have previously demonstrated that all USH1 and 2 proteins in the eye and the inner ear are organized into protein networks by scaffold proteins. This has contributed essentially to our current understanding of the function of USH proteins and explains why defects in proteins of different families cause very similar phenotypes. We have previously shown that the USH1G protein SANS (scaffold protein containing ankyrin repeat…

Scaffold proteinUsher syndromePhosphodiesterase 4D interacting protein (PDE4DIP)Muscle ProteinsPlasma protein bindingMice0302 clinical medicineYeastsChlorocebus aethiopsNuclear proteinCells CulturedGenetics0303 health scienceseducation.field_of_studyNuclear ProteinsCell biologyCOS CellssymbolsPhotoreceptor Cells VertebrateProtein BindingMicrotubule based transportNerve Tissue ProteinsBiologyModels BiologicalRetina03 medical and health sciencessymbols.namesakemedicineAnimalsHumanseducationMolecular BiologyAdaptor Proteins Signal Transducing030304 developmental biologyCell BiologyGlycostation disorders [IGMD 4]Golgi apparatusmedicine.diseaseMacaca mulattaMice Inbred C57BLCytoskeletal ProteinsPhotoreceptor cell functionMyomegalinGenetics and epigenetic pathways of disease Functional Neurogenomics [NCMLS 6]CattleAnkyrin repeatCiliary baseIntracellular transport030217 neurology & neurosurgerySensorineuronal degeneration
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Will it ever become possible to prevent dopaminergic neuronal degeneration?

2008

Parkinsons disease (PD) is the second leading age-related degenerative brain disease in the world affecting millions of people. This neurological disorder disrupts the quality of life of patients and their families, exerts an enormous emotional and physical strain on caregivers, and has a large cost for society. Moreover, the increasing numbers of elderly people in the population will result in a sharp increase in the prevalence of PD. The understanding of its pathophysiology and treatment has advanced at a very impressive rate during past decades. Nevertheless, PD is still fatal and there is at present no cure for it. Furthermore, there are no proven therapies for prevention of PD and alth…

medicine.medical_specialtyDopaminePopulationNeurological disorderDiseaseNeuroprotectionSettore BIO/09 - FisiologiaNeuroprotective agentsRisk FactorsmedicineAnimalsHumansNeuronal degenerationNeurodegeneration Neuroprotection Parkinson's diseaseIntensive care medicineeducationPharmacologyNeuronseducation.field_of_studyCell Deathbusiness.industryGeneral NeuroscienceDopaminergicNeurodegenerative DiseasesParkinson's disease -- Treatmentmedicine.diseaseBrain diseaseNeuroprotective AgentsDrug developmentbusinessNervous system -- Degeneration
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