AimsEvidence for case–control studies suggests that cannabis use is a risk factor for the development of psychosis. However, there have been limited prospective studies and the direction of this association remains controversial. The primary aim of the present study was to examine the association between cannabis use and the incidence of psychotic disorders in people at clinical high risk of psychosis. Secondary aims were to assess associations between cannabis use and the persistence of psychotic symptoms, and with functional outcome.MethodsCurrent and previous cannabis use were assessed in individuals at clinical high risk of psychosis (n = 334) and healthy controls (n = 67), using a modified version of the Cannabis Experience Questionnaire. Participants were assessed at baseline and followed up for 2 years. Transition to psychosis and persistence of psychotic symptoms were assessed using the Comprehensive Assessment of At‐Risk Mental States criteria. Level of functioning at follow up was assessed using the Global Assessment of Functioning disability scale.ResultsDuring follow up, 16.2% of the clinical high‐risk sample developed psychosis. Of those who did not become psychotic, 51.4% had persistent symptoms and 48.6% were in remission. There was no significant association between any measure of cannabis use at baseline and either transition to psychosis, the persistence of symptoms, or functional outcome.ConclusionsThese findings contrast with epidemiological data that suggest that cannabis use increases the risk of psychotic disorder.
BackgroundAlzheimer’s disease (AD) is the most common neurodegenerative disorder and apolipoprotein E (APOE) ε4 allele is the greatest common genetic risk factor for late‐onset AD. In one of the largest multi‐cohort VBM analyses to date, we aimed to a) map regional brain cortical volume deficits in people with dementia vs controls (CTL) and b) investigate how atrophy patterns in AD were modulated by carrying the APOE4 genotype.MethodThe ENIGMA voxel based morphometry (VBM; https://sites.google.com/view/enigmavbm) pipeline was used to perform a mega‐analysis and a multi‐cohort meta‐analysis on T1‐weighted brain MRI data from 1,893 subjects (Table 1) across four different cohorts, namely the Alzheimer’s Disease Neuroimaging Initiative (ADNI), phases 1, GO/2, 3, and the Open Access Series of Imaging Studies (OASIS3). 488 participants with AD had APOE genotype data with 172 non‐carriers (ε3/3) and 316 carriers (ε3/4, ε4/4). Protective APOE ε2 carriers were excluded. Within the 488 participants with AD, effects of carrying the APOE4 allele were tested using a VBM analysis adjusting for age, sex, intracranial volumes and differences in cohorts.ResultAs expected, compared to controls (CTL), participants with dementia demonstrated cortical brain volume deficits in medial temporal lobes, notably the bilateral hippocampus, entorhinal cortex, amygdala and fusiform gyrus in Mega‐ & Meta‐analysis (Fig. 1). In those with AD, APOE4 carriers demonstrated relatively higher gray matter volumes in the primary motor cortex, medial frontal gyrus and posterior middle temporal gyrus, compared to non‐carriers (P<0.001, uncorrected; Fig. 2). As expected, APOE ε4 carriers demonstrated lower medial temporal lobe and precuneal gray matter volumes.ConclusionAn expected strong pattern of medial temporal lobe volume reduction was noted in the dementia group compared to CTL. Interestingly, within the dementia group, APOE ε4 carriers showed higher gray matter density in the primary motor cortex, a region not routinely associated with AD nor with amyloid deposition, as shown in a smaller prior study. APOE ε4 carriers showed typical medial temporal and precuneal volume reductions which commonly show amyloid deposition, consistent with the notion that APOE ε4 mediates atrophy mainly via an amyloid dependent mechanism.References: 1) Ashburner J, Friston KJ. doi:10.1006/nimg.2000.0582. 2) Liu, Ying. doi:10.1016/j.neuron.2014.11.020. 3) La Joie, Renaud. doi:10.1126/scitranslmed.aau5732. 4) Gutiérrez‐Galve L. doi:10.1159/000258100 et al. 2009;28(5):461‐70.
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