Search bioRxivSearch

Biology subjects

Ronan, L.

Publications and source records attributed to Ronan, L..

2 recordsLinked to original sources

Neural correlates of reward anticipation in 2000 children aged 9-10 years: relation to psychotic-like experiences and depressive symptoms

BackgroundSchizophrenia spectrum disorders and depression have been associated with reductions in brain activation during reward anticipation. It is not known whether brain signals associated with reward anticipation relate to psychopathology dimensions of depression or schizophrenia in childhood prior to adolescence.\n\nMethodWe examined whether fMRI brain correlates of reward anticipation related to psychotic-like experiences and symptoms of depression, in 2129 children from the ABCD study aged 9-10 years.Psychotic-like experiences and depression were assessed using the Prodromal Questionnaire Brief Child version and the K-SADS. We fused regional MRI summary statistics for reward anticipation activation in the ABCD study data release 1.0 (contrast of expected large reward versus neutral expectation). Relations between brain activation and psychopathology were assessed using linear regressions in R for 82 brain regions, corrected for multiple comparisons for the number of regions using false discovery rate.\n\nResultsFrom several regressions, there was an isolated unilateral association between right parsorbitalis activation and psychotic-like experiences, but no other significant associations between brain activation and psychopathology.\n\nConclusionsIn 9-10 year old children, reward anticipation is not strongly related to psychotic-like experiences or depression. As previous evidence links depression and schizophrenia to reduced reward anticipation in adults and older adolescents, it appears likely that such associations develop over the adolescent period: this can be tested in follow-up studies of the ABCD cohort.

neuroscience

Pleiotropic effects drive correlation between body mass index and cortical myelination

BackgroundEpidemiological studies have reported significant associations between obesity and neurocognitive decline. Understanding these associations will require deeper analyses of how body mass index (BMI) and brain structure are related. Here we explore the extent to which shared genetic factors (pleiotropy) govern the association between BMI and cortical myelination.\n\nMethodsStatistical models of bivariate heritability were applied to structural MR image data from a cohort of monozyogotic and dizygotic twins. Estimates of phenotypic and genetic correlation between BMI and cortical myelination were derived. A co-twin control design based on monozygotic twins was used to test the hypothesis of a causal relationship between BMI and myelination. The variation in the genetic correlation across the cortex was compared with the average statistical enrichment of genes associated with obesity derived from data from the Allen brain atlas.\n\nResultsStatistically significant phenotypic and genetic correlation between BMI and cortical myelination was observed across the cortex. Taking the heritability of each trait into account, approximately 80% of the phenotypic correlation between the traits was accounted for by shared genetic factors.\n\nIntra-pair differences between traits in monozygotic twins failed to support a causal relationship. Moreover, variation in genetic correlation across the cortex was significantly associated with the statistical enrichment of genes related to obesity.\n\nConclusionsThese results support the hypothesis that pleiotropic effects drive the association between BMI and cortical myelination. This observation may help to explain the co-occurrence of obesity in neurocognitive decline and mental health disorders characterized by changes in myelination and oligodendrocyte function.

neuroscience