0000000000236046

AUTHOR

Christophe Mulle

0000-0003-2709-6615

showing 2 related works from this author

Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

2017

Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated me…

0301 basic medicineMalememoriaAginggenetics [Stress Disorders Post-Traumatic]Diseasegenetics [Neuronal Plasticity]BioinformaticsdemenciaStress Disorders Post-TraumaticMice0302 clinical medicineRisk FactorsNews & ViewsAge of OnsetMice KnockoutNeuronal PlasticitybiologyGeneral NeuroscienceMicrofilament ProteinsNuclear Proteinsgenetics [Nuclear Proteins]FearadultoMiddle AgedAlzheimer's diseasephysiology [Aging]Phenotype3. Good healthPhenotypemiedoFormin 2Forminsgenetics [Aging]estres postraumaticoepidemiology [Stress Disorders Post-Traumatic]AdultHDAC inhibidorpsychology [Dementia]alzheimerForminsNerve Tissue Proteinsepidemiology [Dementia]Affect (psychology)General Biochemistry Genetics and Molecular Biology03 medical and health sciencesHDAC inhibitorMemorygenetics [Dementia]ddc:570medicineDementiaAnimalsHumansenvejecimientoMolecular Biologyphysiology [Memory]General Immunology and MicrobiologyPost-traumatic stress disordermedicine.diseaseYoung age030104 developmental biologyformin 2 protein mouseCase-Control StudiesSynaptic plasticitybiology.proteinDementiagenetics [Microfilament Proteins]complications [Stress Disorders Post-Traumatic]030217 neurology & neurosurgeryHomeostasis
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Mitochondrial CB1 receptors regulate neuronal energy metabolism

2012

The mammalian brain is one of the organs with the highest energy demands, and mitochondria are key determinants of its functions. Here we show that the type-1 cannabinoid receptor (CB(1)) is present at the membranes of mouse neuronal mitochondria (mtCB(1)), where it directly controls cellular respiration and energy production. Through activation of mtCB(1) receptors, exogenous cannabinoids and in situ endocannabinoids decreased cyclic AMP concentration, protein kinase A activity, complex I enzymatic activity and respiration in neuronal mitochondria. In addition, intracellular CB(1) receptors and mitochondrial mechanisms contributed to endocannabinoid-dependent depolarization-induced suppres…

0303 health sciencesCannabinoid receptorCellular respirationGeneral Neurosciencemedicine.medical_treatmentBiologyMitochondrion7. Clean energyEndocannabinoid system3. Good healthCell biology03 medical and health sciences0302 clinical medicinenervous systemMechanism of actionmedicineCannabinoidmedicine.symptomReceptor030217 neurology & neurosurgeryIntracellular030304 developmental biologyNature Neuroscience
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