Objectives. Schizophrenia (SCZ) is associated with disrupted functional brain connectivity, and antipsychotic medications are the primary and most commonly used treatment for schizophrenia. However, not all patients respond to antipsychotic medications. Methods. The study is aimed at investigating whether the graph-theory-based degree centrality (DC), derived from resting-state functional MRI (rs-fMRI), can predict the treatment outcomes. rs-fMRI data from 38 SCZ patients were collected and compared with findings from 38 age- and gender-matched healthy controls (HCs). The patients were treated with antipsychotic medications for 16 weeks before undergoing a second rs-fMRI scan. DC data were processed using DPABI and SPM12 software. Results. SCZ patients at baseline showed increased DC in the frontal and temporal gyrus, anterior cingulate cortex, and precuneus and reduced DC in bilateral subcortical gray matter structures. However, those abnormalities showed a clear renormalization after antipsychotic medication treatments. Support vector machine analysis using leave-one-out cross-validation achieved a correct classification rate of 84.2 (sensitivity 78.9, specificity 89.5, and area under the receiver operating characteristic curve (AUC) 0.925) for differentiating effective subjects from ineffective subjects. Brain areas that contributed most to the classification model were mainly located within the bilateral putamen, left inferior frontal gyrus, left middle occipital cortex, bilateral middle frontal gyrus, left cerebellum, left medial frontal gyrus, left inferior temporal gyrus, and left angular. Furthermore, the DC change within the bilateral putamen is negatively correlated with the symptom improvements after treatment. Conclusions. Our study confirmed that graph-theory-based measures, combined with machine-learning algorithms, can provide crucial insights into pathophysiological mechanisms and the effectiveness of antipsychotic medications.

Working memory (WM) is an essential cognitive function that underpins various higher-order cognitive processes. Improving WM capacity through targeted training interventions has emergered as a potential approach for enhancing cognitive abilities. The present study employed an 8-week regimen of computerized WM training (WMT) to investigate its effect on neuroplasticity in healthy individuals, utilizing neuroimaging data gathered both before and after the training. The key metrics assessed included the amplitude of low-frequency fluctuations (ALFF), voxel-based morphometry (VBM), and the spatial distribution correlations of neurotransmitter. The results indicated that post-training, compared to baseline, there was a reduction in ALFF in the medial superior frontal gyrus and an elevation in ALFF in the left middle occipital gyrus within the training group. In comparison to the control group, the training group also exhibited decreased ALFF in the anterior cingulate cortex, angular gyrus, and superior parietal lobule, along with increased ALFF in the postcentral gyrus post-training. VBM analysis revealed a significant increase in gray matter volume (GMV) in the right dorsal superior frontal gyrus after the training period, compared to the initial baseline measurement. Furthermore, the training group showed GMV increases in the dorsal superior frontal gyrus, Rolandic operculum, precentral gyrus, and postcentral gyrus when compared to the control group. In addition, significant associations were identifed between neuroimaging measurements (AFLL and VBM) and the spatial patterns of neurotransmitters such as serotonin (5-HT), dopamine (DA), and N-methyl-D-aspartate (NMDA), providing insights into the underlying neurochemical processes. These findings clarify the neuroplastic changes caused by WMT, offering a deeper understanding of brain plasticity and highlighting the potential advantages of cognitive training interventions.

Aims: The brain function impairment induced by sleep deprivation (SD) is temporary and can be fully reversed with sufficient sleep. However, in many cases, long‐duration recovery sleep is not feasible. Thus, this study aimed to investigate whether a short nap after SD is sufficient to restore brain function. Methods: The data of 38 subjects, including resting state functional magnetic resonance imaging data collected at three timepoints (before SD, after 30 h of SD, and after a short nap following SD) and psychomotor vigilance task (PVT) data, were collected. Dynamic functional connectivity (DFC) analysis was used to evaluate changes in brain states among three timepoints, and four DFC states were distinguished across the three timepoints. Results: Before SD, state 2 (a resting‐like FC matrix) was dominant (48.26%). However, after 30 h SD, the proportion of state 2 dramatically decreased, and state 3 (still resting‐like, but FCs were weakened) became dominant (40.92%). The increased proportion of state 3 positively correlated with a larger PVT “lapse” time. After a nap, the proportions of states 2 and 3 significantly increased and decreased, respectively, and the change in proportion of state 2 negatively correlated with the change in PVT “lapse” time. Conclusions: Taken together, the results indicated that, after a nap, the cognitive function impairment caused by SD may be reversed to some extent. Additionally, DFC differed among timepoints, which was also associated with the extent of cognitive function impairment after SD (state 3) and the extent of recovery therefrom after a nap (state 2).

Background: It is well known that circadian rhythms and sleep homeostasis contribute to a pronounced trough in sleepiness and behavioral performance at night. However, the underlying neuroimaging mechanisms remain unclear. How brain-function connectivity is modulated during sleep deprivation (SD) has been rarely examined. Methods: By increasing the number of scanning sessions during SD, the current study used voxel-mirrored homotopic connectivity (VMHC) to investigate dynamic changes in interhemispheric communication during one night of SD. Every 2 hours from 10 pm to 06 am (session 1, 10 pm; session 2, 12 am; session 3, 2 am; session 4, 4 am; session 5, 6 am), functional magnetic resonance–imaging data and Stanford Sleepiness Scale (SSS) scores were collected from 36 healthy participants with intermediate chronotype. Dynamic changes in SSS scores and VMHC were determined using one-way repeated-measure ANOVA with the false discovery–rate method to correct for multiple comparisons. Results: Significant time effects for VMHC were found mainly in the bilateral thalamus, bilateral superior temporal gyrus, and bilateral precentral gyrus. SSS scores and VMHC in these areas were both found to be monotonously increased during SD. Furthermore, significant positive associations were found between SSS valu and VMHC values in the left superior temporal and right superior gyri. Conclusion: These findings might represent the dynamic modulation of circadian rhythm merely or the interaction effects of both circadian rhythm and sleep homeostasis on interhemispheric connectivity within the thalamus, default-mode network, and sensorimotor network. Our study provides more comprehensive information on how SD regulates brain connectivity between hemispheres and adds new evidence of neuroimaging correlates of increased sleepiness after SD.

Background: Sleep deprivation (SD) is commonplace in modern society and there are large individual differences in the vulnerability to SD. We aim to identify the structural network differences based on diffusion tensor imaging (DTI) that contribute to the individual different vulnerability to SD. Methods: The number of psychomotor vigilance task (PVT) lapses was used to classify 49 healthy subjects on the basis of whether they were vulnerable or resistant to SD. DTI and graph theory approaches were used to investigate the topologic organization differences of the brain structural connectome between SD‐vulnerable and ‐resistant individuals. We measured the level of global efficiency and clustering in rich club and non‐rich club organizations. Results: We demonstrated that participants vulnerable to SD had less global efficiency, network strength, and local efficiency but longer shortest path length compared with participants resistant to SD. Lower efficiency was mainly distributed in the right insula, bilateral thalamus, bilateral frontal, temporal, and temporal lobes. Furthermore, a disrupted subnetwork was observed that consisted of widespread connections. Moreover, the vulnerable group showed significantly decreased strength of the rich club compared with the resistant group. The strength of rich club connectivity was found to be correlated negatively with PVT performance ( r = −0.395, p = 0.005). We further tested the reliability of the results. Conclusion: The findings revealed that individual differences in resistance to SD are related to disrupted topologic efficiency connectome pattern, and our study may provide potential connectome‐based biomarkers for the early detection of the vulnerable degree to SD.