Journal of Psychiatry & Neuroscience最新文献

Background: Panic disorder is a common disabling condition with limited biomarkers. We aimed to explore the diagnostic and treatment response prediction value of functional temporal variability in people with panic disorder.

Methods: Patients with panic disorder and healthy controls received resting-state functional magnetic resonance imaging scans and assessments. After 2 weeks of treatment, the patients with panic disorder were divided into remitted (RPD; n = 39) or nonremitted (NRPD; n = 43) subgroups. Baseline temporal variability was analyzed between the panic disorder and control groups as well as between RPD and NRPD subgroups.

Results: Our sample included 82 patients with panic disorder (39 RPD, 43 NRPD) and 105 controls. The panic disorder group showed decreased temporal variability in the left posterior cingulate gyrus (PCG), right lingual gyrus, right fusiform gyrus, and right thalamus (all p < 0.05, Bonferroni-corrected). A combination of variability in the lingual gyrus, PCG, and thalamus had optimal predictive value for distinguishing between the panic disorder and control groups (area under the curve = 0.776, sensitivity = 0.781, specificity = 0.732). In addition, the RPD subgroup showed significantly lower temporal variability in the left insula, right PCG, and bilateral lingual gyrus than the NRPD subgroup and control group (all p < 0.05, Bonferroni-corrected). Variability in the left insula and left lingual gyrus negatively correlated with the reduction rate of panic symptoms (all p < 0.05, Bonferroni-corrected).

Limitations: Functional brain images were collected only at baseline and may have been affected by medication use. Also, the follow-up period was only 2 weeks; sustained clinical remission may require longer follow-up.

Conclusion: Combining lingual gyrus, PCG, and thalamus temporal variability alterations helped distinguish patients with panic disorder from healthy controls. The temporal variability in the insula and lingual gyrus are potential biomarkers for the treatment of panic disorder.

Background: Reduced glutamatergic excitability of the anterior cingulate cortex (ACC) has been long suspected in schizophrenia; recent observations support low glutamatergic tone as the primary pathophysiology contributing to subtle early features of this illness, with a secondary disinhibition (higher glutamate tone) resulting in more prominent clinical symptoms later in its course. We sought to investigate whether people with genetic high risk (GHR) for schizophrenia have lower glutamate levels in the ACC than those at later stages of clinical high risk (CHR) and those with first-episode schizophrenia (FES), among whom symptoms are already prominent.

Methods: We recruited people with CHR, GHR, or FES, as well as healthy controls. Using proton magnetic resonance spectroscopy, we determined glutamate levels in the perigenual ACC (pACC) and dorsal ACC (dACC) using a 3 T scanner.

Results: We recruited 302 people across multiple stages of psychosis, including 63 with CHR, 76 with GHR, and 96 with FES, as well as 67 healthy controls. Those with GHR had lower glutamate levels in the dACC than those with CHR, while those with CHR had higher glutamate levels in the pACC than those with FES. Higher disorganization, but not any other symptom domain, was associated with lower levels of glutamate in the GHR group (dACC and pACC) and in the CHR group (pACC).

Limitations: The cross-sectional design precluded inferences regarding individual clinical trajectory and resolution at 3 T was insufficient to separate spectra of glutamine from glutamate.

Conclusion: Reduced glutamatergic tone among people genetically predisposed to schizophrenia supports diminished excitability as an early feature of schizophrenia, contributing to the subtle symptom of disorganization across high-risk states. Higher glutamate levels become apparent when psychotic symptoms become prominent, possibly as a disinhibitory effect and, at the full-blown stage of psychosis, the relationship between glutamate concentrations and symptoms ceases to be simply linear.

Background: Deficient neural activities during emotion regulation have been reported in depression. We sought to conduct a meta-analysis to provide a comprehensive description of these neural alterations during use of emotion regulation strategies among patients with depression, including major depressive disorder (MDD) and bipolar disorder (BD).

Methods: We identified neuroimaging studies of abnormal neural activities during emotion regulation in depression. We extracted the peak coordinates and effect sizes of differences in brain activity between patients and healthy controls. Using seed-based d mapping, we conducted voxel-wise meta-analyses of the neural activation pattern differences between the 2 groups across conditions involving emotion regulation and those where emotion regulation was not needed.

Results: We included 33 studies reporting 34 data sets, including 23 involving MDD (571 people with MDD and 578 matched controls) and 11 involving BD (358 people with BD and 369 matched controls). Overall, compared with controls, patients with depression showed hyperactivity in the insula and postcentral gyrus, and hypoactivity in the prefrontal part of the inferior, middle, and superior frontal gyrus, the middle temporal gyrus, and the supplementary motor area. In subgroup analyses, data from patients with MDD and studies focused on decreasing negative emotions or using the emotional strategy of reappraisal reported specific hypoactivity in the middle cerebellar peduncles.

Limitations: Given limited studies involving patients with BD, we were unable to detect the common and distinct abnormalities in neural activation between MDD and BD. We did not conduct any meta-regression analyses because of limited information.

Conclusion: In this meta-analysis, we identified hyperactivity in brain regions associated with emotional experience and hypoactivity in brain regions associated with cognitive control during emotion regulation among patients with depression, relative to healthy controls. These findings could help indicate a target for future interventions aimed at increasing emotion regulation capacity for patients with depression.

Background: The underlying functional alterations of brain structural changes among patients with empathy impairment following stroke remain unclear. We sought to investigate functional connectivity changes informed by brain structural abnormalities in multimodal magnetic resonance imaging (MRI) among patients with empathy impairment following stroke.

Methods: We enrolled people who had experienced their first ischemic stroke, along with healthy controls. We assessed empathy 3 months after stroke using the Chinese version of the Empathy Quotient (EQ). During the acute phase, all patients underwent basic magnetic resonance imaging (MRI), followed by multimodal MRI during follow-up. Our MRI analyses encompassed acute infarction segmentation, volumetric brain measurements, regional quantification of diffusion parameters, and both region-of-interest-based and seed-based functional connectivity assessments. We grouped patients based on the severity of their empathy impairment for comparative analysis.

Results: We included 84 patients who had stroke and 22 healthy controls. Patients had lower EQ scores than controls. Patients with low empathy had larger left cortical infarcts (odds ratio [OR] 4.082, 95% confidence interval [CI] 1.183-14.088), more pronounced atrophy in the right cingulate cortex (OR 1.248, 95% CI 1.038-1.502), and lower scores on the Montreal Cognitive Assessment (OR 0.873, 95% CI 0.74-0.947). In addition, the cingulate cortex served as the seed in the seed-based analysis, which showed heightened functional connectivity between the anterior cingulate gyrus and the right superior parietal lobule, specifically in the low-empathy group.

Limitations: We did not evaluate the relationship between specific network involvement and empathy impairment among patients following stroke.

Conclusion: Among patients with subacute ischemic stroke, reduced empathy was strongly associated with a more severe cognitive profile and atrophy of the right cingulate cortex. Our subsequent structural-informed functional MRI analysis suggests that the enhanced connectivity between the anterior cingulate gyrus and the superior parietal lobule may function as a compensatory mechanism for this atrophy.

Background: Adult hippocampal neurogenesis has been extensively characterized in rodent models, but its existence in humans remains controversial. We sought to assess the phenomenon in postmortem human hippocampal samples by combining spatial transcriptomics and multiplexed fluorescent in situ hybridization.

Methods: We computationally examined the spatial expression of various canonical neurogenesis markers in postmortem dentate gyrus (DG) sections from young and middle-aged sudden-death males. We conducted in situ assessment of markers expressed in neural stem cells, proliferative cells, and immature granule neurons in postmortem DG sections from infant, adolescent, and middle-aged males.

Results: We examined frozen DG tissue from infant (n = 1, age 2 yr), adolescent (n = 1, age 16 yr), young adult (n = 2, mean age 23.5 yr), and middle-aged (n = 2, mean age 42.5 yr) males, and frozen-fixed DG tissue from middle-aged males (n = 6, mean age 43.5 yr). We detected very few cells expressing neural stem cell and proliferative markers in the human DG from childhood to middle age. However, at all ages, we observed a substantial number of DG cells expressing the immature neuronal marker DCX. Most DCX ⁺ cells displayed an inhibitory phenotype, while the remainder were non-committed or excitatory in nature.

Limitations: The study was limited by small sample sizes and included samples only from males.

Conclusion: Our findings indicate very low levels of hippocampal neurogenesis throughout life and the existence of a local reserve of plasticity in the adult human hippocampus. Overall, our study provides important insight into the distribution and phenotype of cells expressing neurogenesis markers in the adult human hippocampus.

Background: Increasing evidence suggests an important role of the gut microbiome in the pathogenesis of mental disorders, including depression, along the microbiota-gut-brain axis. We sought to explore the interactions between gut microbe composition and neural circuits in late-life depression (LLD).

Methods: We performed fecal 16S ribosomal RNA (rRNA) sequencing and resting-state functional magnetic resonance imaging in a case-control cohort of older adults with LLD and healthy controls to characterize the association between gut microbiota and brain functional connectivity (FC). We used the Hamilton Depression Rating Scale (HAMD) to assess depressive symptoms.

Results: We included 32 adults with LLD and 16 healthy controls. At the genus level, the relative abundance of Enterobacter, Akkermansiaceae, Hemophilus, Burkholderia, and Rothia was significantly higher among patients with LDD than controls. Reduced FC within mood regulation circuits was mainly found in the frontal cortex (e.g., the right superior and inferior frontal gyrus, right lateral occipital cortex, left middle frontal gyrus, and left caudate) among patients with MDD. Group-characterized gut microbes among controls and patients showed opposite correlations with seed-based FC, which may account for the aberrant emotion regulation among patients with LDD. The abundance of Enterobacter (dominant genus among patients with LLD) was positively correlated with both HAMD scores (r = 0.49, p = 0.0004) and group-characterized FC (r = -0.37, p < 0.05), while Odoribacter (dominant genus among controls) was negatively correlated with both HAMD scores (r = -0.30, p = 0.04) and group-characterized FC.

Limitations: The study's cross-sectional design and small sample size limit causal inferences; larger longitudinal studies are required for detailed subgroup analyses.

Conclusion: We identified significant correlations between LDD-characterized gut microbes and brain FC, as well as depression severity, which may contribute to the pathophysiology of depression development among patients with LLD. Specific microbes were linked to altered brain connectivity, suggesting potential targets for treating LLD.

For 3000 years, psychedelics have been used in religious contexts to enhance spiritual thinking, well-being, and a sense of community. In the last few years, a renaissance in the use of psychedelic drugs for mental disorders has occurred in Western society; consequently, a pressing scientific need to elucidate the intricate mechanisms underlying their actions has arisen. Psychedelics mainly bind to serotonin (5-HT) receptors, particularly 5-HT_2A receptors, but may also bind to other receptors. Unlike conventional psychotropic drugs used in psychiatry, psychedelics introduce a distinctive complexity. They not only engage in receptor activation, but also exert influence over specific neural circuits, thereby facilitating transformative cognitive experiences and fostering what many have identified as a spiritual contemplation or mystical experience. This comprehensive review describes clinical studies that have examined the propensity of psychedelics to enhance spiritual, mystical, and transcendent cognitive states. This multifaceted nature, encompassing diverse components and paradigms, necessitates careful consideration during the investigation of psychedelic mechanisms of action to avoid oversimplification. The present review endeavours to elucidate the mechanisms underlying the actions of 2 principal psychedelic substances, psilocybin and lysergic acid diethylamide (LSD), with a focus on monoamine and glutamate receptor mechanisms; molecular aspects, such as neuroplasticity and epigenetics; as well as the impact of psychedelics on brain circuits, including the default mode network and the cortico-striato-thalamo-cortical network. Given their distinctive and intricate mechanisms of action, psychedelics necessitate a novel conceptual framework in psychiatry, offering insight into the treatment of mental health disorders and facilitating the integration of the realms of brain, mind, and spirituality.