0000000000869657

AUTHOR

Regina Hanstein

showing 4 related works from this author

Increased Connexin 43 Expression as a Potential Mediator of the Neuroprotective Activity of the Corticotropin-Releasing Hormone

2009

CRH is a major central stress mediator, but also a potent neuroprotective effector. The mechanisms by which CRH mediates its neuroprotective actions are largely unknown. Here, we describe that the gap junction molecule connexin43 (Cx43) mediates neuroprotective effects of CRH toward experimentally induced oxidative stress. An enhanced gap junction communication has been reported to contribute to neuroprotection after neurotoxic insults. We show that CRH treatment up-regulates Cx43 expression and gap junctional communication in a CRH receptor-dependent manner in IMR32 neuroblastoma cells, primary astrocytes, and organotypic hippocampal slice cultures. MAPKs and protein kinase A-cAMP response…

medicine.medical_specialtyendocrine systemCorticotropin-Releasing HormoneMAP Kinase Signaling SystemCarbenoxoloneConnexinBiologyNeuroprotectionModels BiologicalArticleRats Sprague-DawleyCorticotropin-releasing hormoneMiceEndocrinologyMediatorInternal medicineCell Line Tumormedicinepolycyclic compoundsAnimalsHumansProtein kinase AMolecular BiologyGap junctionBrainGap JunctionsGeneral MedicineCell biologyRatsEndocrinologyNeuroprotective Agentsnervous systemGene Expression RegulationConnexin 43cardiovascular systemSignal transductionhormones hormone substitutes and hormone antagonistsmedicine.drugSignal Transduction
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Effects of neuron-specific ADAM10 modulation in an in vivo model of acute excitotoxic stress.

2008

A disintegrin and metalloprotease (ADAM) 10 is the main candidate enzyme for the alpha-secretase processing of the amyloid precursor protein (APP). Neuron-specific ADAM10 overexpression proved beneficial in the APP[V717I] mutant Alzheimer mouse model [Postina R, Schroeder A, Dewachter I, Bohl J, Schmitt U, Kojro E, Prinzen C, Endres K, Hiemke C, Blessing M, Flamez P, Dequenne A, Godaux E, van Leuven F, Fahrenholz F (2004) A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model. J Clin Invest 113:1456-1464]. Since Alzheimer patients have a high prevalence for epileptic seizures, we investigated the effects of ADAM10 modula…

Genetically modified mousemedicine.medical_specialtyIndolesADAM10TransgeneExcitotoxicityMice Transgenicmedicine.disease_causeNeuroprotectionHippocampusADAM10 ProteinAmyloid beta-Protein PrecursorMiceLeucineSeizuresStress PhysiologicalInternal medicineGlial Fibrillary Acidic ProteinmedicineAmyloid precursor proteinAnimalsNeuroinflammationNeuronsAnalysis of VarianceKainic AcidbiologyCell DeathDose-Response Relationship DrugChemistryGeneral NeuroscienceNeurodegenerationMembrane ProteinsValinemedicine.diseaseADAM ProteinsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinAmyloid Precursor Protein SecretasesPlant LectinsNeuroscienceNeuroscience
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Cannabinoid receptor 1 deficiency in a mouse model of Alzheimer's disease leads to enhanced cognitive impairment despite of a reduction in amyloid de…

2012

Alzheimer's disease (AD) is characterized by amyloid-beta deposition in amyloid plaques, neurofibrillary tangles, inflammation, neuronal loss, and cognitive deficits. Cannabinoids display neuromodulatory and neuroprotective effects and affect memory acquisition. Here, we studied the impact of cannabinoid receptor type 1 (CB1) deficiency on the development of AD pathology by breeding amyloid precursor protein (APP) Swedish mutant mice (APP23), an AD animal model, with CB1-deficient mice. In addition to the lower body weight of APP23/CB1(-/-) mice, most of these mice died at an age before typical AD-associated changes become apparent. The surviving mice showed a reduced amount of APP and its …

Agingmedicine.medical_specialtyPathologyCannabinoid receptormedicine.medical_treatmentMutantMice TransgenicInflammationDiseaseNeuroprotectionAmyloid beta-Protein PrecursorMiceReceptor Cannabinoid CB1Alzheimer DiseaseCell Line TumorInternal medicinemental disordersmedicineAmyloid precursor proteinAnimalsHumansMaze LearningCognitive impairmentAmyloid beta-Peptidesbiologybusiness.industryGeneral NeuroscienceBody WeightAge FactorsBrainPeptide FragmentsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinlipids (amino acids peptides and proteins)MicrogliaNeurology (clinical)CannabinoidGeriatrics and Gerontologymedicine.symptomCognition DisordersbusinessDevelopmental BiologyNeurobiology of Aging
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Transgenic overexpression of corticotropin releasing hormone provides partial protection against neurodegeneration in an in vivo model of acute excit…

2008

Abstract Corticotropin releasing hormone (CRH) is the central modulator of the mammalian hypothalamic–pituitary–adrenal (HPA) axis. In addition, CRH affects other processes in the brain including learning, memory, and synaptic plasticity. Moreover, CRH has been shown to play a role in nerve cell survival under apoptotic conditions and to serve as an endogenous neuroprotectant in vitro . Employing mice overexpressing murine CRH in the CNS, we observed a differential response of CRH-overexpressing mice (CRH-COE hom -Nes) to acute excitotoxic stress induced by kainate compared with controls (CRH-COE con -Nes). Interestingly, CRH-overexpression reduced the duration of epileptic seizures and pre…

endocrine systemmedicine.medical_specialtyIndolesRNA UntranslatedCorticotropin-Releasing HormoneExcitotoxicityMice TransgenicNerve Tissue ProteinsBiologymedicine.disease_causeNeuroprotectionHippocampusNestinCorticotropin-releasing hormoneMiceIntermediate Filament ProteinsNeurotrophic factorsNeurofilament ProteinsSeizuresInternal medicineGlial Fibrillary Acidic Proteinpolycyclic compoundsmedicineExcitatory Amino Acid AgonistsReaction TimeAnimalsNeuroinflammationBrain-derived neurotrophic factorAnalysis of VarianceKainic AcidCell DeathGeneral NeuroscienceBrain-Derived Neurotrophic FactorNeurodegenerationProteinsLong-term potentiationmedicine.diseaseDisease Models AnimalEndocrinologynervous systemGene Expression RegulationNerve DegenerationNeurotoxicity SyndromesPlant Lectinshormones hormone substitutes and hormone antagonistsNeuroscience
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