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O'Hora, K. P.

Publications and source records attributed to O'Hora, K. P..

5 recordsLinked to original sources

Convergent and Divergent Cerebellar Alterations in 22q11.2 Copy Number Variants

BackgroundIndividuals with copy number variants (CNVs) at 22q11.2 are at elevated risk for neurodevelopmental and psychiatric disorders, including autism spectrum disorder and intellectual disability. For psychosis, effects diverge, with 22q11.2 deletion (22qDel) conferring one of the highest known risks for schizophrenia, while duplication (22qDup) may be protective. Prior investigations of neurobiological mechanisms in 22q11.2 CNVs have predominantly focused on the cerebrum, whereas the cerebellum--a region increasingly recognized for its contributions to cognitive, affective, and social processes--remains underexplored and represents a promising target for investigation. Although alterations in cerebellar structure have been reported in 22qDel, they remain largely unexplored in 22qDup. This study provides the first characterization of regional cerebellar volumes in 22qDup and the first direct comparison of cerebellar structure across 22q11.2 CNVs, offering a unique opportunity to identify shared and distinct neurobiological mechanisms with implications for understanding cerebellar contributions to brain-behavior relationships in CNV carriers. MethodsWe analyzed 514 longitudinally collected structural Magnetic Resonance Imaging (MRI) scans of 111 individuals with 22qDel, 37 individuals with 22qDup, and 167 typically developing (TD) controls. Total and regional cerebellar volumes were quantified using ACAPULCO, a deep-learning-based parcellation method that segments the cerebellum into 28 subregions. Group differences in cerebellar volumes, as well as their associations with cognition, autism-related traits, and psychosis-risk symptoms, were examined using linear mixed-effects models. False discovery rate (FDR) correction was applied to control for multiple comparisons where appropriate. ResultsIn relation to TD controls, cerebellar volumes were broadly reduced in 22qDel, whereas cerebellar alterations in 22qDup were more modest and variable. Regional analyses revealed both linear (22qDel < TD < 22qDup) and nonlinear (22qDel {approx} 22qDup < TD; 22qDel < 22qDup < TD) gene-dosage patterns, though not all reached significance. Vermis VII was significantly reduced in both CNVs but showed no relationship to behavioral differences. In contrast, reduction of Right Lobule VIIIA was associated with greater social impairment in 22qDup. Unlike TD controls, this region was not associated with IQ in 22qDup, suggesting CNV-specific alterations in cerebellar-behavior relationships. ConclusionThese findings indicate that reciprocal CNVs at the 22q11.2 locus both affect cerebellar structure, yet their functional consequences diverge, suggesting overlapping but distinct pathways to clinical risk. They underscore the cerebellums multifaceted role in neurodevelopment and highlight the need for studies examining broader cognitive and socio-affective domains, as well as cerebellar-cortical connectivity, to clarify links to clinical outcomes.

neuroscience↗

Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion

22q11.2 deletion (22qDel) and duplication (22qDup) carriers have an increased risk of neurodevelopmental disorders and exhibit altered brain structure, including white matter microstructure. However, the underlying cellular architecture and age-related changes contributing to these white matter alterations remain poorly understood. Neurite orientation dispersion and density imaging (NODDI) was used on mixed cross-sectional and longitudinal data to examine group differences and age-related trajectories in measures of axonal density (i.e., intracellular volume fraction; ICVF), axonal orientation (orientation dispersion index; ODI) and free water diffusion (isotropic volume fraction; ISO) in 50 22qDel (n scans = 69, mean age = 20.7, age range = 7.4-51.1, 64.0% female) and 24 22qDup (n scans = 34, mean age = 21.6, age range = 8.3-49.4, 54.2% female) carriers, and 890 controls (n scans = 901, mean age = 21.9, age range = 7.8-51.1, 54.5% female). The results showed widespread gene dosage effects, with higher ICVF in 22qDel and lower ICVF in 22qDup compared to controls, and region-specific effects of the 22qDel and 22qDup on ODI and ISO measures. However, 22qDel and 22qDup carriers did not exhibit altered age-related trajectories relative to controls. Observed differences in ICVF suggest higher white matter axonal density in 22qDel and lower axonal density in 22qDup compared to controls. Conversely, differences in ODI are highly localized, indicating region-specific effects on axonal dispersion in white matter. We do not find evidence for altered developmental trajectories of axonal density or dispersion among 22q11.2 CNV carriers, suggesting stable disruptions to neurodevelopmental events before childhood.

neuroscience↗

Unique functional neuroimaging signatures of genetic versus clinical high risk for psychosis

Background22q11.2 Deletion Syndrome (22qDel) is a copy number variant (CNV) associated with psychosis and other neurodevelopmental disorders. Adolescents at clinical high risk for psychosis (CHR) have subthreshold psychosis symptoms without known genetic risk factors. Whether common neural substrates underlie these distinct high-risk populations is unknown. We compared functional brain measures in 22qDel and CHR cohorts and mapped results to biological pathways. MethodsWe analyzed two large multi-site cohorts with resting-state functional MRI (rs-fMRI): 1) 22qDel (n=164, 47% female) and typically developing (TD) controls (n=134, 56% female); 2) CHR individuals (n=244, 41% female) and TD controls (n=151, 46% female) from the North American Prodrome Longitudinal Study-2. We computed global brain connectivity (GBC), local connectivity (LC), and brain signal variability (BSV) across cortical regions, testing case-control differences for 22qDel and CHR separately. Group difference maps were related to published brain maps using autocorrelation-preserving permutation. ResultsBSV, LC, and GBC are significantly disrupted in 22qDel compared with TD controls (False Discovery Rate q<0.05). Spatial maps of BSV and LC differences are highly correlated with each other, unlike GBC. In CHR, only LC is significantly altered versus controls, with a different spatial pattern compared to 22qDel. Group differences map onto biological gradients, with 22qDel effects strongest in regions with high predicted blood flow and metabolism. Conclusion22qDel and CHR exhibit divergent effects on fMRI temporal variability and multi-scale functional connectivity. In 22qDel, strong and convergent disruptions in BSV and LC not seen in CHR individuals suggest distinct functional brain alterations.

neuroscience↗

Effects of Gene Dosage and Development on Subcortical Nuclei Volumes in Individuals with 22q11.2 Copy Number Variations

The 22q11.2 locus contains genes critical for brain development. Reciprocal Copy Number Variations (CNVs) at this locus impact risk for neurodevelopmental and psychiatric disorders. Both 22q11.2 deletions (22qDel) and duplications (22qDup) are associated with autism, but 22qDel uniquely elevates schizophrenia risk. Understanding brain phenotypes associated with these highly penetrant CNVs can provide insights into genetic pathways underlying neuropsychiatric disorders. Human neuroimaging and animal models indicate subcortical brain alterations in 22qDel, yet little is known about developmental differences across specific nuclei between reciprocal 22q11.2 CNV carriers and typically developing (TD) controls. We conducted a longitudinal MRI study in 22qDel (n=96, 53.1% female), 22qDup (n=37, 45.9% female), and TD controls (n=80, 51.2% female), across a wide age range (5.5-49.5 years). Volumes of the thalamus, hippocampus, amygdala, and anatomical subregions were estimated using FreeSurfer, and the effect of 22q11.2 gene dosage was examined using linear mixed models. Age-related changes were characterized with general additive mixed models (GAMMs). Positive gene dosage effects (22qDel < TD < 22qDup) were observed for total intracranial and whole hippocampus volumes, but not whole thalamus or amygdala volumes. Several amygdala subregions exhibited similar positive effects, with bi-directional effects found across thalamic nuclei. Distinct age- related trajectories were observed across the three groups. Notably, both 22qDel and 22qDup carriers exhibited flattened development of hippocampal CA2/3 subfields relative to TD controls. This study provides novel insights into the impact of 22q11.2 CNVs on subcortical brain structures and their developmental trajectories.

neuroscience↗

Longitudinal development of thalamocortical functional connectivity in 22q11.2 deletion syndrome

Background22q11.2 Deletion Syndrome (22qDel) is a genetic Copy Number Variant (CNV) that strongly increases risk for schizophrenia and other neurodevelopmental disorders. Disrupted functional connectivity between the thalamus and somatomotor/frontoparietal cortex has been implicated in cross-sectional studies of 22qDel, idiopathic schizophrenia, and youth at clinical high risk (CHR) for psychosis. Here, we use a novel functional atlas approach to investigate longitudinal age-related changes in network-specific thalamocortical functional connectivity (TCC) in 22qDel and typically developing (TD) controls. MethodsTCC was calculated for nine functional networks derived from resting-state functional magnetic resonance imaging (rs-fMRI) scans collected from n=65 22qDel participants (63.1% female) and n=69 demographically matched TD controls (49.3% female), ages 6 to 23 years. Analyses included 86 longitudinal follow-up scans. Non-linear age trajectories were characterized with general additive mixed models (GAMMs). ResultsIn 22qDel, TCC in the frontoparietal network increases until approximately age 13, while somatomotor and cingulo-opercular TCC decrease from age 6 to 23. In contrast, no significant relationships between TCC and age were found in TD controls. Somatomotor connectivity in 22qDel is significantly higher than TD in childhood, but lower in late adolescence. Frontoparietal TCC shows the opposite pattern. Conclusions22qDel is associated with aberrant development of functional network connectivity between the thalamus and cortex. Younger individuals with 22qDel have lower frontoparietal connectivity and higher somatomotor connectivity than controls, but this phenotype may normalize or partially reverse by early adulthood. Altered maturation of this circuitry may underlie elevated neuropsychiatric disease risk in this syndrome.

neuroscience↗