15 research outputs found
Extraversion is linked to volume of the orbitofrontal cortex and amygdala
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103145.pdf (publisher's version ) (Open Access)Neuroticism and extraversion are personality factors associated with the vulnerability for developing depression and anxiety disorders, and are possibly differentially related to brain structures implicated in the processing of emotional information and the generation of mood states. To date, studies on brain morphology mainly focused on neuroticism, a dimension primarily related to negative affect, yielding conflicting findings concerning the association with personality, partially due to methodological issues and variable population samples under study. Recently, extraversion, a dimension primarily related to positive affect, has been repeatedly inversely related to with symptoms of depression and anxiety disorders. In the present study, high resolution structural T1-weighted MR images of 65 healthy adults were processed using an optimized Voxel Based Morphometry (VBM) approach. Multiple regression analyses were performed to test for associations of neuroticism and extraversion with prefrontal and subcortical volumes. Orbitofrontal and right amygdala volume were both positively related to extraversion. Extraversion was differentially related to volume of the anterior cingulate cortex in males (positive) and females (negative). Neuroticism scores did not significantly correlate with these brain regions. As extraversion is regarded a protective factor for developing anxiety disorders and depression and has been related to the generation of positive affect, the present results indicate that the reduced likelihood of developing affective disorders in individuals high on extraversion is related to modulation of emotion processing through the orbitofrontal cortex and the amygdala.6 p
Characterization and origin of large Campanian depressions within the Chalk Group of the Danish Central Graben – implications for hydrocarbon exploration and development
CARABAS : a database for carbonates body geometries
Rebelle Michel, Friedenberg R., Boichard R., Leroy E., Szambelanczyk J., Van buchem Frans S. P. CARABAS : a database for carbonates body geometries. In: Géologie Méditerranéenne. Tome 28, numéro 1-2, 2001. Anatomy of Carbonate Bodies / Anatomie des corps carbonates. International Meeting / Colloque international. Marseille, 9-12 mai 2001, France, sous la direction de Marc Floquet, Jérôme Hennuy et Jean-Pierre Masse. pp. 149-154
Évolution paléo-environnementale et écologique au Barrémien-Aptien du sous-bassin de Galve (Espagne)
Embry Jean-Christophe, Vennin Emmanuelle, Van buchem Frans S. P., Pierre Catherine, Schroeder Rolf, Aurell Marcos. Évolution paléo-environnementale et écologique au Barrémien-Aptien du sous-bassin de Galve (Espagne). In: Documents des Laboratoires de Géologie, Lyon, n°156, 2002. STRATI 2002. 3ème congrès français de stratigraphie. Lyon, 8-10 juillet 2002. pp. 104-105
Seismic chronostratigraphy and basin development at a Mid-Cretaceous intrashelf basin margin
Correlation of messinian carbonate platforms
Esteban M., Clauzon Georges, Cornée Jean-Jacques, Cunningham K., Ferrandini Jean, Franseen E., Görür Naci, Guieu Gérard, Grasso M., Hôffling R., Meyers N., Muller J., Pedley Martyn, Plaziat J.-Cl., Suballyuva A., Suc Jean-Pierre, Valleri G., Van buchem Frans S. P. Correlation of messinian carbonate platforms. In: Géologie Méditerranéenne. Tome 21, numéro 1-2, 1994. Récifs et plates-formes carbonatées miocènes de Méditerranée / Miocene reefs and carbonate platforms of the Mediterranean. Interim colloquium R.C.M.N.S. (Marseille 3-6 mai 1994) sous la direction de Jean-Paul Saint-Martin et Jean-Jacques Cornée. pp. 159-163
Cerebrovascular and amyloid pathology in predementia stages: the relationship with neurodegeneration and cognitive decline
Prevalence of the apolipoprotein E epsilon 4 allele in amyloid beta positive subjects across the spectrum of Alzheimer's disease
Introduction: Apolipoprotein E (APOE) epsilon 4 is the major genetic risk factor for Alzheimer's disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid beta(A beta) pathology. Methods: We included 3451 A beta+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE epsilon 4 prevalence in relation to age, sex, education, and geographical location. Results: The APOE epsilon 4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in A beta+ cognitively normal and A beta+ mild cognitive impairment (P <.05) but not in A beta+ AD dementia (P =.66). The prevalence was highest in Northern Europe but did not vary by sex or education. Discussion: The APOE E4 prevalence in AD was higher than that in previous studies, which did not require presence of A beta pathology. Furthermore, our results highlight disease heterogeneity related to age and geographical location. (C) 2018 the Alzheimer's Association. Published by Elsevier Inc. All rights reserved
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Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis.
ImportanceCerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies.ObjectiveTo use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI).Data sourcesRelevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE and Web of Science databases and through personal communication with investigators.Study selectionStudies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity.Data extraction and synthesisIndividual records were provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies.Main outcomes and measuresPrevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations.ResultsThe prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95% CI, 8%-13%) to 44% (95% CI, 37%-51%) among participants with normal cognition; from 12% (95% CI, 8%-18%) to 43% (95% CI, 32%-55%) among patients with SCI; and from 27% (95% CI, 23%-32%) to 71% (95% CI, 66%-76%) among patients with MCI. APOE-ε4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ε4ε4 carriers, 50 years for ε2ε4 carriers, 55 years for ε3ε4 carriers, 65 years for ε3ε3 carriers, and 95 years for ε2ε3 carriers. Amyloid positivity was more common in highly educated participants but not associated with sex or biomarker modality.Conclusions and relevanceAmong persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. These findings suggest a 20- to 30-year interval between first development of amyloid positivity and onset of dementia