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Schizophrenia is associated with robust hippocampal volume deficits but subregion volume deficits, their associations with cognition, and contributing genes remain to be determined.
Hippocampal formation (HF) subregion volumes were obtained using FreeSurfer 6.0 from individuals with schizophrenia (n = 176, mean age ± s.d. = 39.0 ± 11.5, 132 males) and healthy volunteers (n = 173, mean age ± s.d. = 37.6 ± 11.3, 123 males) with similar mean age, gender, handedness, and race distributions. Relationships between the HF subregion volume with the largest between group difference, neuropsychological performance, and single-nucleotide polymorphisms were assessed.
This study found a significant group by region interaction on hippocampal subregion volumes. Compared to healthy volunteers, individuals with schizophrenia had significantly smaller dentate gyrus (DG) (Cohen's d = −0.57), Cornu Ammonis (CA) 4, molecular layer of the hippocampus, hippocampal tail, and CA 1 volumes, when statistically controlling for intracranial volume; DG (d = −0.43) and CA 4 volumes remained significantly smaller when statistically controlling for mean hippocampal volume. DG volume showed the largest between group difference and significant positive associations with visual memory and speed of processing in the overall sample. Genome-wide association analysis with DG volume as the quantitative phenotype identified rs56055643 (β = 10.8, p < 5 × 10−8, 95% CI 7.0–14.5) on chromosome 3 in high linkage disequilibrium with MOBP. Gene-based analyses identified associations between SLC25A38 and RPSA and DG volume.
This study suggests that DG dysfunction is fundamentally involved in schizophrenia pathophysiology, that it may contribute to cognitive abnormalities in schizophrenia, and that underlying biological mechanisms may involve contributions from MOBP, SLC25A38, and RPSA.
Studies have produced conflicting evidence regarding whether cognitive
control deficits in patients with schizophrenia result from dysfunction
within the cognitive control network (CCN; top-down) and/or unisensory
To investigate CCN and sensory cortex involvement during multisensory
cognitive control in patients with schizophrenia.
Patients with schizophrenia and healthy controls underwent functional
magnetic resonance imaging while performing a multisensory Stroop task
involving auditory and visual distracters.
Patients with schizophrenia exhibited an overall pattern of response
slowing, and these behavioural deficits were associated with a pattern of
patient hyperactivation within auditory, sensorimotor and posterior
parietal cortex. In contrast, there were no group differences in
functional activation within prefrontal nodes of the CCN, with small
effect sizes observed (incongruent–congruent trials). Patients with
schizophrenia also failed to upregulate auditory cortex with concomitant
increased attentional demands.
Results suggest a prominent role for dysfunction within auditory,
sensorimotor and parietal areas relative to prefrontal CCN nodes during
multisensory cognitive control.
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