0000000000786591

AUTHOR

José J. Lucas

0000-0003-1597-3916

showing 2 related works from this author

GSK3β overexpression induces neuronal death and a depletion of the neurogenic niches in the dentate gyrus

2010

Overexpression of GSK3β in transgenic mice induces learning deficits and some features associated with Alzheimer's disease (AD), including dentate gyrus (DG) atrophy. Here, we assessed whether these mice also recapitulate DG atrophy as well as impaired neurogenesis reported in AD. Ultrastructural analysis revealed that there were fewer and more disorganized neurogenic niches in these animals, coupled with an increase in the proportion of immature neurons. Indeed, the maturation of granule cells is delayed as witnessed by the alterations to the length and patterning of their dendritic trees and to the mossy fiber terminals. Together with an increase in neuronal death, these phenomena lead to…

Genetically modified mouseProgrammed cell deathOverexpressionNeurogenesisproliferationCognitive NeuroscienceCellular differentiationeducationProliferationMice TransgenicBiologyGlycogen Synthase Kinase 3MiceAtrophyAlzheimer DiseaseMaturationmedicineAnimalsHumanshippocampal stem cellsGSK3Bhealth care economics and organizationsCell ProliferationGlycogen Synthase Kinase 3 betaCell DeathMicrogliamaturationDentate gyrusNeurogenesisGSK3 betaCell DifferentiationAlzheimer's diseasemedicine.diseaseMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureHippocampal stem cellsDentate GyrusGSK3bMicrogliaAlzheimer’s diseaseNeuroscienceoverexpressionHippocampus
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Loss of striatal type 1 cannabinoid receptors is a key pathogenic factor in Huntington's disease.

2010

Endocannabinoids act as neuromodulatory and neuroprotective cues by engaging type 1 cannabinoid receptors. These receptors are highly abundant in the basal ganglia and play a pivotal role in the control of motor behaviour. An early downregulation of type 1 cannabinoid receptors has been documented in the basal ganglia of patients with Huntington's disease and animal models. However, the pathophysiological impact of this loss of receptors in Huntington's disease is as yet unknown. Here, we generated a double-mutant mouse model that expresses human mutant huntingtin exon 1 in a type 1 cannabinoid receptor-null background, and found that receptor deletion aggravates the symptoms, neuropatholog…

MaleHuntingtinCannabinoid receptorCell Survivalmedicine.medical_treatmentBlotting WesternMice TransgenicBiologyMotor ActivityGrowth Hormone-Releasing HormoneMiceReceptor Cannabinoid CB1medicineCannabinoid receptor type 2AnimalsDronabinolReceptorBrain-derived neurotrophic factorNeuronsAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemMagnetic Resonance ImagingCorpus StriatumHuntington DiseaseRotarod Performance TestGPR18Neurology (clinical)CannabinoidNeuroscienceBrain : a journal of neurology
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