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The human face plays a central role in emotions and social communication. The emotional and somatic motor networks generate facial behaviors, but whether facial behaviors have representations in the structural anatomy of the human brain is unknown. We coded 16 facial behaviors in 55 healthy older adults who viewed five videos that elicited emotions and examined whether individual differences in facial behavior were related to regional variation in gray matter volume. Voxel-based morphometry analyses revealed that greater emotional facial behavior during the disgust trial (i.e. greater brow furrowing and eye tightening as well as nose wrinkling and upper lip raising) and the amusement trial (i.e. greater smiling and eye tightening) was associated with larger gray matter volume in midcingulate cortex, supplementary motor area, and precentral gyrus, areas spanning both the emotional and somatic motor networks. When measured across trials, however, these facial behaviors (and others) only related to gray matter volume in the precentral gyrus, a somatic motor network hub. These findings suggest that the emotional and somatic motor networks store structural representations of facial behavior and that the midcingulate cortex is critical for generating the predictable movements in the face that arise during emotions.

The relationship between neurotransmitters and oxidative stress in Major Depressive Disorder (MDD) patients, considering HPA axis activity and psychological and cognitive states, is unclear. This study examines changes in neurotransmitters (GABA, Glx) and antioxidants (GSH) in the dorsal anterior cingulate cortex (dACC) of MDD patients under varying levels of ACTH, and their relationship with psychological and cognitive conditions. Forty-five MDD patients were divided into high-ACTH (>65 pg/mL; n = 16) and normal-ACTH (7–65 pg/mL; n = 29) groups based on blood ACTH levels, along with 12 healthy controls (HC). All participants underwent HAM-D, HAM-A assessments, and most completed MMSE and MoCA tests. GABA+, Glx, and GSH levels in the dACC were measured using the MEGA-PRESS sequence. Intergroup differences and correlations between clinical factors, HPA axis activity, and metabolites were analyzed. Compared to HC, the normal ACTH group showed higher Glx and lower GSH levels. Glx and GSH were negatively correlated with MDD severity. In the high-ACTH MDD group, Glx positively correlated with delayed memory, and GSH positively correlated with abstraction. Factors influencing GABA included ACTH levels, depression duration, and negative events. Predictive factors for HAM-D scores were GSH and GABA. The sample size is small. MDD patients exhibit neurochemical differences in the brain related to HPA axis levels, MDD severity, and cognitive function. Clinical factors, neurotransmitters, and neuroendocrine levels significantly influence depression severity. [Display omitted] • Compared to healthy controls, the normal ACTH MDD patients had higher Glx and lower GSH levels • Glx and GSH levels were inversely related to MDD severity • In the high ACTH MDD group, Glx positively correlated with delayed memory, and GSH with abstraction • Neurochemical differences in MDD patients' brains at varying HPA axis levels are linked to MDD severity and cognitive function [ABSTRACT FROM AUTHOR]

Although there are a few first-line treatment options for bipolar depression, none are rapid-acting. A new rTMS protocol, Stanford Accelerated Intelligent Neuromodulation Therapy (SAINT®), has been shown to have a rapid antidepressant effect in major depressive disorder (MDD). We examined the preliminary safety, tolerability, and efficacy of SAINT for the treatment of depression in a small sample of persons with treatment-resistant bipolar I disorder. Participants with treatment-resistant bipolar I disorder currently experiencing moderate to severe depression were treated with open-label SAINT. Resting-state functional MRI (fMRI) was used to generate individualized treatment targets for each participant based on the region of the left dorsolateral prefrontal cortex most anticorrelated with the subgenual anterior cingulate cortex. Participants were treated with 10 iTBS sessions daily, with 50-min intersession intervals, for up to 5 consecutive days. The primary outcome was change in Montgomery-Åsberg Depression Rating Scale (MADRS) from baseline to immediate follow-up after treatment. We treated 10 participants and found a mean reduction of 16.9 in MADRS scores, with a 50 % response rate and 40 % remission rate immediately following treatment. 60 % of participants met remission criteria within the 1-month period following treatment. No serious adverse events, manic episodes, or cognitive side effects were observed. Our study has a limited sample size and larger samples are needed to confirm safety and efficacy. SAINT has shown preliminary feasibility, safety, tolerability, and efficacy in treating treatment-resistant bipolar I depression. Double-blinded sham-controlled trials with larger samples are needed to confirm safety and efficacy. • A novel TMS protocol, SAINT, showed rapid antidepressant effect in bipolar I patients. • Stanford-developed, SAINT, was successfully used at two other academic hospitals. • No signs of mania or negative cognitive side effects were observed. [ABSTRACT FROM AUTHOR]

Depression is a significant public health concern. Identifying biopsychosocial risk factors for depression is important for developing targeted prevention. Studies have demonstrated that blunted striatal activation during reward processing is a risk factor for depression; however, few have prospectively examined whether adolescent reward-related resting-state functional connectivity (rsFC) predicts depression symptoms in adulthood and how this relates to known risk factors (e.g., childhood trauma). At baseline, 66 adolescents (mean age = 14.7, SD = 1.4, 68 % female) underwent rsFC magnetic resonance imaging and completed the Children's Depression Inventory (CDI). At follow-up (mean time between adolescent scan and adult follow-up = 10.1 years, SD = 1.6, mean adult age = 24.8 years, SD = 1.7), participants completed the Childhood Trauma Questionnaire (CTQ) and Beck Depression Inventory– Second Edition (BDI-2). Average rsFC was calculated between nodes in mesocorticolimbic reward circuitry: ventral striatum (VS), rostral anterior cingulate cortex (rACC), medial orbitofrontal cortex, and ventral tegmental area. Linear regressions assessed associations between rsFC, BDI-2, and CTQ, controlling for adolescent CDI, sex assigned at birth, and scan age (Bonferroni corrected). Greater childhood trauma was associated with higher adulthood depression symptoms. Stronger VS-rACC rsFC during adolescence was associated with greater depression symptoms in adulthood and greater childhood trauma. The small sample size, limited depression severity, and seed-based approach are limitations. The associations between adolescent striatal-cingulate rsFC and childhood trauma and adult depression symptoms suggest this connectivity may be an early neurobiological risk factor for depression and that early life experience plays an important role. Increased VS-rACC connectivity may represent an over-regulatory response on the striatum, commonly reported in depression, and warrants further investigation. • Depression rates are rising and childhood trauma is a risk factor for depression. • Trauma-exposed and depressed populations show reward-related neural aberrations. • Adolescent reward-related neural aberrations were related to adulthood depression. • Childhood trauma was associated with the same adolescent neural aberrations. • Further investigation of biopsychosocial risk factors of depression is needed. [ABSTRACT FROM AUTHOR]

Different brain areas have distinct roles in the processing and regulation of pain and thus may form specific pharmacological targets. Prior research has shown that AMPAkines, a class of drugs that increase glutamate signaling, can enhance descending inhibition from the prefrontal cortex (PFC) and nucleus accumbens. On the other hand, activation of neurons in the anterior cingulate cortex (ACC) is known to produce the aversive component of pain. The impact of AMPAkines on ACC, however, is not known. We found that direct delivery of CX516, a well-known AMPAkine, into the ACC had no effect on the aversive response to pain in rats. Furthermore, AMPAkines did not modulate the nociceptive response of ACC neurons. In contrast, AMPAkine delivery into the prelimbic region of the prefrontal cortex (PL) reduced pain aversion. These results indicate that the analgesic effects of AMPAkines in the cortex are likely mediated by the PFC but not the ACC. [ABSTRACT FROM AUTHOR]

Introduction: In a variety of behavioral procedures animals will show selective fear responding in shock-associated contexts, but not in other contexts. However, several factors can lead to generalized fear behavior, where responding is no longer constrained to the conditioning context and will transfer to novel contexts. Methods: Here, we assessed memory generalization using an inhibitory avoidance paradigm to determine if generalized avoidance behavior engages the retrosplenial cortex (RSC). Male and female Long Evans rats received inhibitory avoidance training prior to testing in the same context or a shifted context in two distinct rooms; one room that had fluorescent lighting (Light) and one that had red LED lighting (Dark). Results: We found that animals tested in a light context maintained context-specificity; animals tested in the same context as training showed longer latencies to cross and animals tested in the shifted context showed shorter latencies to cross. However, animals tested in the dark generalized their avoidance behavior; animals tested in the same context and animals tested in the shifted context showed similarly-high latencies to cross. We next examined expression of the immediate early gene zif268 and perineuronal nets (PNNs) following testing and found that while activity in the basolateral amygdala corresponded with overall levels of avoidance behaviors, anterior RSC (aRSC) activity corresponded with learned avoidance generally, but posterior RSC (pRSC) activity seemed to correspond with generalized memory. PNN reduction in the RSC was associated with memory formation and retrieval, suggesting a role for PNNs in synaptic plasticity. Further, PNNs did not reduce in the RSC in animals who showed a generalized avoidance behavior, in line with their hypothesized role in memory consolidation. Discussion: These findings suggest that there is differential engagement of retrosplenial subregions along the rostrocaudal axis to generalization and discrimination. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM) seriously threatens human health and the quality of life, cognitive impairment is considered as a common complication of T2DM. Neuroimaging meta-analysis found brain functional and structural abnormality in patients with T2DM. Therefore, the purpose of the meta-analysis was to identify brain regions of patients with T2DM-related cognitive impairment (T2DM-CI) where functional and structural indicators changed together or could not synchronize. A literature screening of neuroimaging studies on cognitive impairment in T2DM was conducted from 1 January 2007 to 26 May 2023 in PubMed, Web of Science, Cochrane Library, and Medline databases. The functional indicators we studied were amplitude of low-frequency fluctuation (ALFF), regional homogeneity (ReHo) and degree centrality (DC), while the structural indicator was gray matter (GM), which included gray matter volume (GMV) and cerebral cortical thickness. Studies reporting ALFF, ReHo, DC and GM abnormalities between T2DM-CI and healthy controls (HCs) were selected and their significant peak coordinates (x, y, z) and effect size (t-value) were extracted to perform a meta-analysis using anisotropic effect size sign differential mapping (AES-SDM) 5.15 software. Moreover, the brain regions with significant differences obtained from meta-analysis were saved as masks and then validated in our data. Total 19 studies and 20 datasets were involved in this study. Compared to HCs, combining ALFF, ReHo, and DC measurements, the brain activity of the left anterior cingulate/paracingulate gyri (ACC.L, BA24) in T2DM-CI patients increased significantly, while the brain activity of the left lingual gyrus (LING.L, BA18) in T2DM-CI patients decreased significantly. The GM indicator of the right superior temporal gyrus (STG.R, BA42) and left inferior occipital gyrus (IOG.L, BA19) in T2DM-CI patients decreased significantly. Meta-regression analysis showed the negative relationship between the brain activity reduction in LING.L and the percentage of female patients, as well as the negative relationship between GM reduction in IOG.L and T2DM duration. Furthermore, we validated a decrease in brain activity in the LING.L of T2DM-CI patients in our independent dataset. The decrease of brain activity in LING.L and the decrease of GM in IOG.L were closely related to visual impairment in T2DM-CI patients. These abnormal brain regions may be the main targets for future research, early intervention can delay the further development of cognitive impairment in T2DM patients and improve their quality of life, which also provided early biomarkers for clarifying the mechanism of cognitive impairment in T2DM. [ABSTRACT FROM AUTHOR]

Pupil dynamics has emerged as a critical non-invasive indicator of brain state changes. In particular, pupillary-light-responses (PLR) in Alzheimer's disease (AD) patients show potential as biomarkers for brain degeneration. To investigate AD-specific PLR and its underlying neuromodulatory sources, we combine high-resolution awake mouse fMRI with real-time pupillometry to map brain-wide event-related correlation patterns based on illumination-driven pupil constriction ( P c ) and post-illumination pupil dilation recovery (amplitude, P d , and time, T). The P c -driven differential analysis reveals altered visual signal processing and reduced thalamocortical activation in AD mice in comparison with wild-type (WT) control mice. In contrast, the post-illumination pupil dilation recovery-based fMRI highlights multiple brain areas associated with AD brain degeneration, including the cingulate cortex, hippocampus, septal area of the basal forebrain, medial raphe nucleus, and pontine reticular nuclei (PRN). Additionally, the brain-wide functional connectivity analysis highlights the most significant changes in PRN of AD mice, which serves as the major subcortical relay nuclei underlying oculomotor function. This work integrates non-invasive pupil-fMRI measurements in preclinical models to identify pupillary biomarkers based on brain-wide functional changes, including neuromodulatory dysfunction coupled with AD brain degeneration. This work applies high-resolution fMRI with real-time pupillometry in 5xFAD transgenic mice to verify pupillary biomarkers of Alzheimer's disease (AD). In particular, the pupil-driven fMRI maps identify dysfunction of neuromodulatory pathways affected by AD degeneration. [ABSTRACT FROM AUTHOR]

Objective: Mild cognitive impairment (MCI) is a common non-motor manifestation of Parkinson's disease, commonly referred to as PD-MCI. However, there is a lack of comprehensive data regarding the role of glial cell line-derived neurotrophic factor (GDNF) and cerebral white matter damage in the pathogenesis of PD-MCI. The objective of this study is to investigate the association between alterations in GDNF levels and cerebral white matter damage in individuals diagnosed with PD-MCI, as well as to explore their potential involvement in cognitive progression. Methods: Neuropsychological assessments were conducted on 105 patients with Parkinson's disease and 45 healthy volunteers to examine various cognitive domains. An enzyme-linked immunosorbent assay (ELISA) was employed to measure serum levels of GDNF. Additionally, all participants underwent 3.0T magnetic resonance imaging (MRI) to acquire diffusion tensor images (DTI), and a voxel-based analysis (VBA) approach was utilized to compare the fractional anisotropy (FA) values of white matter in the brain. Results: There was a significant correlation between the right corpus callosum, right cingulate gyrus, and the Digit Span Backward Test (DSB-T) as well as the Trail Making Test A (TMT-A), both of which assess attention and working memory functions. The left internal capsule exhibited a significant correlation with the Trail Making Test B (TMT-B) and the Clock Drawing Test (CDT), which evaluate executive function. Additionally, the right cingulate gyrus showed a significant association with scores on the Auditory Verbal Learning Test-HuaShan (AVLT-H), assessing memory function. Abnormal fiber structures that demonstrated significant correlations with serum GDNF levels included the left internal capsule, left corticospinal tract, right corpus callosum, and right cingulate gyrus. Conclusion: The decrease in serum GDNF levels among PD-MCI patients exhibiting impairments in attention and working memory function was significantly correlated with alterations in the corpus callosum (knee) and posterior cingulate gyrus. Furthermore, the reduction of serum GDNF levels in PD-MCI patients with impaired executive function is associated with changes in the internal capsule (forelimb) projection fibers. Additionally, the decline of serum GDNF levels in PD-MCI patients experiencing memory function impairment is related to alterations in the right cingulate gyrus. [ABSTRACT FROM AUTHOR]

Background and Purpose: Neuropathic pain (NP) is a debilitating condition following spinal cord injury (SCI). The role of periaqueductal gray (PAG) in NP development following SCI remains underexplored. Using resting‐state functional MRI (rsfMRI), our study aimed to demonstrate the alterations in functional connectivity (FC) of PAG in NP following SCI. Methods: Ten SCI patients (SCI + NP, n = 7, and SCI − NP, n = 3), alongside 10 healthy controls (HCs), were enrolled. rsfMRI was conducted followed by seed‐to‐voxel analysis using PAG as the seed region and then group‐based analysis comprising three groups (SCI + NP, SCI − NP, and HC). Age and gender were considered as confounding variables. Results: Compared to HCs, SCI + NP demonstrated decreased FC between PAG and right insula, right frontal orbital cortex, right pallidum, dorsal raphe nucleus (DRN), red nuclei (RN), substantia nigra (SN), and ventral posterolateral (VPL) thalamic nuclei. Compared to SCI − NP, SCI + NP demonstrated increased FC between PAG and posterior cingulate cortex (PCC), hippocampus, cerebellar vermis lobules IV and V, and thalamic structures (posterior and lateral pulvinar, the mediodorsal nuclei, and the ventral lateral nuclei). Additionally, decreased FC between the PAG and VPL, geniculate bodies, intralaminar nuclei of thalamus, DRN, RN, SN, and prefrontal cortex was observed in this comparison. Conclusions: Altered FC between PAG and right anterior insula, VPL, DRN, RN, SN, cerebellar vermis lobules IV and V, frontal cortex, and PCC was associated with NP sequelae of SCI. Additionally, SCI was independently associated with decreased FC between PAG and right posterior insula, cerebellar lobules IV and V, and cerebellar vermis lobules III, IV, and V. [ABSTRACT FROM AUTHOR]

Background: Cannabidiol (CBD) impacts brain regions implicated in anxiety reactivity and stress reactivity (e.g., amygdala, anterior cingulate cortex (ACC), anterior insula (AI)); however, placebo-controlled studies are mixed regarding CBD's anxiolytic effects. We previously reported that CBD expectancy alone can alter subjective, physiological, and endocrine markers of stress/anxiety; however, it is unclear whether these findings reflect altered brain reactivity. This study evaluated whether CBD expectancy independently alters amygdala resting-state functional connectivity (rsFC) with the ACC and AI following acute stress. Method: Thirty-eight (20 females) healthy adults were randomly assigned to receive accurate or inaccurate information regarding the CBD content of a CBD-free oil administered during a single experimental session. Following a baseline resting state MRI scan, participants administered their assigned oil sublingually, engaged in a stress task (serial subtraction with negative feedback) inside the scanner, and underwent another resting state MRI scan. Amygdala rsFC with the ACC and AI was measured during each scan, and the subjective state was assessed at six time points. Outcomes were analyzed using ANCOVA. Results: CBD expectancy (vs CBD-free expectancy) was associated with significantly weaker rsFC between the left amygdala and right ACC (p = 0.042), but did not systematically alter amygdala-AI rsFC (p- values > 0.05). We also replicated our previously reported CBD expectancy effects on subjective stress/anxiety in the scanner context. Conclusion: CBD placebo effects may be sufficient to alter neural responses relevant to its purported anxiolytic and stress-relieving properties. Future work is needed to replicate these results and determine whether CBD expectancy and pharmacology interact to alter neural anxiety reactivity and stress reactivity. [ABSTRACT FROM AUTHOR]

Objective Methods Results Interpretation We prospectively studied asymptomatic C9orf72 mutation carriers, identifying those developing amyotrophic lateral sclerosis (ALS) or frontotemporal dementia (FTD).We enrolled 56 asymptomatic family members (AFM) with a C9orf72 mutation (AFM C9+), 132 non‐carriers (AFM C9−), and 359 population‐based controls. Using 3 T magnetic resonance imaging, we measured cortical thickness, gyrification, and subcortical volumes longitudinally. Linear mixed‐effects models on non‐converting AFM C9+ scans (n = 107) created a reference for these measurements, establishing individual atrophy patterns. Atrophy patterns from presymptomatic phenoconverters (n = 10 scans) served as a template for group comparisons and similarity assessments. Similarity with phenoconverters was quantified using Dice similarity coefficient (DSC) for cortical and Kullback–Leibler similarity (KLS) for subcortical measures. Using longitudinal similarity assessments, we predicted when participants would reach the average similarity level of phenoconverters at their first post‐onset scan.Five AFM C9+ converted to ALS or ALS‐FTD. Up to 6 years before symptoms, these phenoconverters exhibited significant atrophy in frontal, temporal, parietal, and cingulate cortex, along with smaller thalamus, hippocampus, and amygdala compared to other AFM C9+. Some non‐converted AFM C9+ had high DSC and KLS, approaching values of phenoconverters, whereas others, along with AFM C9− and controls, had lower values. At age 80, we predicted 27.9% (95% confidence interval, 13.2–40.1%) of AFM C9+ and no AFM C9− would reach the same DSC as phenoconverters.Distinctive atrophy patterns are visible years before symptom onset on presymptomatic scans of phenoconverters. Combining baseline and follow‐up similarity measures may serve as a promising imaging biomarker for identifying those at risk of ALS or ALS‐FTD. ANN NEUROL 2024 [ABSTRACT FROM AUTHOR]

Schizophrenia is a severe psychiatric disorder associated with brain alterations at rest. Amplitude of low-frequency fluctuations (ALFF) and its fractional version (fALFF) have been widely used to investigate alterations in spontaneous brain activity in schizophrenia. However, results are still inconsistent. Furthermore, while these measurements are similar, they showed some differences, and no meta-analysis has been yet performed to compare them in schizophrenia. Thus, we conducted systematic research in five databases and in the grey literature to find articles investigating fALFF and/or ALFF alterations in schizophrenia. Two separate meta-analyses were performed using the SDM-PSI software to identify fALFF and ALFF alterations separately. Then, a conjunction analysis was conducted to determine congruent results between the two approaches. We found that patients with schizophrenia showed altered fALFF activity in the left insula/putamen, the right paracentral lobule and the left middle occipital gyrus compared to healthy individuals. Patients with schizophrenia exhibited ALFF alterations in the bilateral putamen, the bilateral caudate nucleus, the bilateral inferior frontal gyrus, the right precuneus, the right precentral gyrus, the left postcentral gyrus, the right posterior cingulate gyrus, compared to healthy controls. ALFF increased activity in the left putamen was higher in drug-naïve patients and was correlated with positive symptoms. The conjunction analysis revealed a spatial convergence between fALFF and ALFF studies in the left putamen. This left putamen cluster is part of the associative striatum. Its alteration in schizophrenia provides additional support to the influential aberrant salience hypothesis of psychosis. [ABSTRACT FROM AUTHOR]

This study aims to elucidate the neuroimaging changes associated with major depressive disorder (MDD) and their relationship with genetic characteristics. We conducted a global-brain functional connectivity (GFC) and genetic-neuroimaging correlation analysis on 42 MDD patients and 42 healthy controls (HCs), exploring the correlation between GFC abnormalities and clinical variables. Results showed that compared to HCs, MDD patients had significantly decreased GFC values in the bilateral posterior cingulate cortex/precuneus and increased GFC values in the left and right cerebellum Crus I/II. Additionally, a negative correlation was observed between the GFC values of the left cerebellum Crus I/II and subjective support scores, as well as social support revalued scale total scores. We identified genes associated with GFC changes in MDD, which are enriched in biological processes such as synaptic transmission and ion transport. Our findings indicate the presence of abnormal GFC values in severe depression, complementing the pathological research on the condition. Furthermore, this study provides preliminary evidence for the correlation between social support levels and brain functional connectivity, offering insights into the potential association between GFC changes and gene expression in MDD patients. [ABSTRACT FROM AUTHOR]

The anterior cingulate cortex (ACC) plays a crucial role in the perception of pain. It is consistently activated by noxious stimuli and its hyperactivity in chronic pain indicates plasticity in the local neuronal network. However, the way persistent pain effects and modifies different neuronal cell types in the ACC and how this contributes to sensory sensitization is not completely understood. This study confirms the existence of 2 primary subtypes of pyramidal neurons in layer 5 of the rostral, agranular ACC, which we could classify as intratelencephalic (IT) and cortico-subcortical (SC) projecting neurons, similar to other cortical brain areas. Through retrograde labeling, whole-cell patch-clamp recording, and morphological analysis, we thoroughly characterized their different electrophysiological and morphological properties. When examining the effects of peripheral inflammatory pain on these neuronal subtypes, we observed timedependent plastic changes in excitability. During the acute phase, both subtypes exhibited reduced excitability, which normalized to pre-inflammatory levels after day 7. Daily conditioning with nociceptive stimuli during this period induced an increase in excitability specifically in SC neurons, which was correlated with a decrease in mechanical sensitization. Subsequent inhibition of the activity of SC neurons projecting to the periaqueductal gray with in vivo chemogenetics, resulted in reinstatement of the hypersensitivity. Accordingly, it was sufficient to enhance the excitability of these neurons chemogenetically in the inflammatory pain condition to induce hypoalgesia. These findings suggest a cell type–specific effect on the descending control of nociception and a cellular mechanism for pain-induced analgesia. Furthermore, increased excitability in this neuronal population is hypoalgesic rather than hyperalgesic. [ABSTRACT FROM AUTHOR]

The retrosplenial cortex (RSC) is a key component of the brain's memory systems, with anatomical connections to the hippocampus, anterior thalamus, and entorhinal cortex. This circuit has been implicated in episodic memory and many of these structures have been shown to encode temporal information, which is critical for episodic memory. For example, hippocampal time cells reliably fire during specific segments of time during a delay period. Although RSC lesions are known to disrupt temporal memory, time cells have not been observed there. In this study, we reanalyzed archival RSC neuronal firing data during the intertrial delay period from two previous experiments involving different behavioral tasks, a blocked alternation task and a cued T‐maze task. For the blocked alternation task, rats were required to approach the east or west arm of a plus maze for reward during different blocks of trials. Because the reward locations were not cued, the rat had to remember the goal location for each trial. In the cued T‐maze task, the reward location was explicitly cued with a light and the rats simply had to approach the light for reward, so there was no requirement to hold a memory during the intertrial delay. Time cells were prevalent in the blocked alternation task, and most time cells clearly differentiated the east and west trials. We also found that RSC neurons could exhibit off‐response time fields, periods of reliably inhibited firing. Time cells were also observed in the cued T‐maze, but they were less prevalent and they did not differentiate left and right trials as well as in the blocked alternation task, suggesting that RSC time cells are sensitive to the memory demands of the task. These results suggest that temporal coding is a prominent feature of RSC firing patterns, consistent with an RSC role in episodic memory. [ABSTRACT FROM AUTHOR]

Background: The subgenual gyrus is a promising target for deep brain stimulation (DBS) against depression. However, to optimize this treatment modality, we need translational animal models. Aim: To describe the anatomy and connectivity of the Göttingen minipig subgenual area (sgC). Materials and methods: The frontal pole of 5 minipigs was cryosectioned into 40 μm coronal and horizontal sections and stained with Nissl and NeuN-immunohistochemistry to visualize cytoarchitecture and cortical lamination. Eight animals were unilaterally stereotaxically injected in the sgC with anterograde (BDA) and retrograde (FluoroGold) tracers to reveal the sgC connectivity. Results: In homology with human nomenclature (Brodmann 1909), the minipig sgC can be subdivided into three distinct areas named area 25 (BA25), area 33 (BA33), and indusium griseum (IG). BA25 is a thin agranular cortex, approximately 1 mm thick. Characteristically, perpendicular to the pial surface, cell-poor cortical columns separate the otherwise cell-rich cortex of layer II, III and V. In layer V the cells are of similar size as seen in layer III, while layer VI contains more widely dispersed neurons. BA33 is less differentiated than BA25. Accordingly, the cortex is thinner and displays a complete lack of laminar differentiation due to diffusely arranged small, lightly stained neurons. It abuts the IG, which is a neuron-dense band of heavily stained small neurons separating BA33 directly from the corpus callosum and the posteriorly located septal nuclear area. Due to the limited area size and nearby location to the lateral ventricle and longitudinal cerebral fissure, only 3/8 animals received sgC injections with an antero- and retrograde tracer mixture. Retrograde tracing was seen primarily to the neighbouring ipsilateral ventral- and mPFC areas with some contralateral labelling as well. Prominent projections were furthermore observed from the ipsilateral insula, the medial aspect of the amygdala and the hippocampal formation, diencephalon and the brainstem ventral tegmental area. Anterograde tracing revealed prominent projections to the neighbouring medial prefrontal, mPFC and cingulate cortex, while moderate staining was noted in the hippocampus and adjoining piriform cortex. Conclusion: The minipig sgC displays a cytoarchitectonic pattern and connectivity like the human and may be well suited for further translational studies on BA25-DBS against depression. [ABSTRACT FROM AUTHOR]

With increasing numbers of magnetic resonance imaging (MRI) datasets becoming publicly available, researchers and clinicians alike have turned to automated methods of segmentation to enable population-level analyses of these data. Although prior research has evaluated the extent to which automated methods recapitulate "gold standard" manual segmentation methods in the human brain, such an evaluation has not yet been carried out for segmentation of MRIs of the macaque brain. Macaques offer the important opportunity to bridge gaps between microanatomical studies using invasive methods like tract tracing, neural recordings, and high-resolution histology and non-invasive macroanatomical studies using methods like MRI. As such, it is important to evaluate whether automated tools derive data of sufficient quality from macaque MRIs to bridge these gaps. We tested the relationship between automated registration-based segmentation using an open source and actively maintained NHP imaging analysis pipeline (AFNI) and gold standard manual segmentation of 4 structures (2 cortical: anterior cingulate cortex and insula; 2 subcortical: amygdala and caudate) across 37 rhesus macaques (Macaca mulatta). We identified some variability in the strength of correlation between automated and manual segmentations across neural regions and differences in relationships with demographic variables like age and sex between the two techniques. [ABSTRACT FROM AUTHOR]

The subdivisions of the extended cingulate cortex of the human brain are implicated in a number of high-level behaviors and affected by a range of neuropsychiatric disorders. Its anatomy, function, and response to therapeutics are often studied using non-human animals, including the mouse. However, the similarity of human and mouse frontal cortex, including cingulate areas, is still not fully understood. Some accounts emphasize resemblances between mouse cingulate cortex and human cingulate cortex while others emphasize similarities with human granular prefrontal cortex. We use comparative neuroimaging to study the connectivity of the cingulate cortex in the mouse and human, allowing comparisons between mouse 'gold standard' tracer and imaging data, and, in addition, comparison between the mouse and the human using comparable imaging data. We find overall similarities in organization of the cingulate between species, including anterior and midcingulate areas and a retrosplenial area. However, human cingulate contains subareas with a more fine-grained organization than is apparent in the mouse and it has connections to prefrontal areas not present in the mouse. Results such as these help formally address between-species brain organization and aim to improve the translation from preclinical to human results. [ABSTRACT FROM AUTHOR]

Background: Perinatal depression (PND) is a debilitating condition affecting maternal well‐being and child development. Allopregnanolone (ALLO) is important to perinatal neuroplasticity, however its relationship with depression severity and postpartum structural brain volume is unknown. Method: We examined perinatal temporal dynamics and bidirectional associations between ALLO and depression severity and the association between these variables and postpartum gray matter volume, using a random intercept cross‐lagged panel model. Results: We identified a unidirectional predictive relationship between PND severity and ALLO concentration, suggesting greater depression severity early in the perinatal period may contribute to subsequent changes in ALLO concentration (β = 0.26, p = 0.009), while variations in ALLO levels during the perinatal period influences the development and severity of depressive symptoms later in the postpartum period (β = 0.38, p = 0.007). Antepartum depression severity (Visit 2, β = 0.35, p = 0.004), ALLO concentration (Visit 2, β = 0.37, p = 0.001), and postpartum depression severity (Visit 3, β = 0.39, p = 0.031), each predicted the right anterior cingulate volume. Antepartum ALLO concentration (Visit 2, β = 0.29, p = 0.001) predicted left suborbital sulcus volume. Antepartum depression severity (Visit 1, β = 0.39, p = 0.006 and Visit 2, β = 0.48, p < 0.001) predicted the right straight gyrus volume. Postpartum depression severity (Visit 3, β = 0.36, p = 0.001) predicted left middle‐posterior cingulate volume. Conclusion: These results provide the first evidence of bidirectional associations between perinatal ALLO and depression severity with postpartum gray matter volume. [ABSTRACT FROM AUTHOR]

Opioid use disorder is a chronic relapsing disorder. The brain adapts to opioids that are taken for pain treatment or recreational use so that abstinence becomes a true challenge for individuals with opioid use disorder. Studying brain dysfunction at this stage is difficult, and human neuroimaging has provided highly heterogeneous information. Here, we took advantage of an established mouse model of morphine abstinence together with functional magnetic resonance imaging to investigate whole-brain functional connectivity (FC) first at rest and then in response to an acute morphine challenge during image acquisition. Hierarchical clustering of seed pair correlation coefficients showed modified FC in abstinent animals, brainwide and regardless of the condition. Seed-to-voxel analysis and random forest classification, performed on data at rest, indicated that the retrosplenial cortex (a core component of the default mode network) and the amygdala (a major aversion center) are the best markers of abstinence, thus validating the translatability of the study. Seed pair network clustering confirmed disruption of a retrosplenial cortex–centered network, reflecting major reorganization of brain FC. The latter analysis also identified a persistent but unreported morphine signature in abstinent mice at rest, which involves cortical and midbrain components and characterizes the enduring morphine footprint. Finally, dynamic FC analysis revealed that the intrascanner acute morphine challenge modified FC faster and more broadly in abstinent animals, demonstrating brainwide adaptations of FC reactivity to an acute opioid challenge. This study used a unique experimental design to demonstrate that a prior history of chronic opioid exposure leaves a durable pharmacological signature on brain communication, with implications for pain management and recovery from opioid use disorder. [ABSTRACT FROM AUTHOR]

Borderline personality disorder (BPD) is a severe mental illness, with high rates of co-morbid depression and suicidality. Despite the importance of optimizing treatment in BPD, little is known about how neural processes relate to individual treatment response. This study examines how baseline regional brain blood oxygen level dependent (BOLD) activation during a functional magnetic resonance imaging (fMRI) task of emotion regulation is related to treatment response following a six-month randomized clinical trial of Dialectical Behavior Therapy (DBT) or Selective Serotonin Reuptake Inhibitor (SSRI) treatment. Unmedicated females with BPD (N = 37), with recent suicidal behavior or self-injury, underwent an fMRI task in which negative personal memories were presented and they were asked to distance (i.e., downregulate their emotional response) or immerse (i.e., experience emotions freely). Patients were then randomized to DBT (N = 16) or SSRI (N = 21) treatment, with baseline and post-treatment depression and BPD severity assessed. BOLD activity in prefrontal cortex, anterior cingulate, and insula was associated with distancing. Baseline BOLD during distancing in dorsolateral, ventrolateral, and orbital prefrontal cortex (dlPFC, vlPFC, OFC) differentially predicted depression response across treatment groups, with higher activity predicting better response in the SSRI group, and lower activity predicting better response in the DBT group. All female samples. Findings indicate that greater prefrontal engagement during emotion regulation may predict more antidepressant benefit from SSRIs, whereas lower engagement may predict better response to DBT. These results suggest different mechanisms of action for SSRI and DBT treatment, and this may allow fMRI to guide individualized treatment selection. • Borderline personality disorder (BPD) is associated with high rates of depression. • Neural processes may offer insight into predicting antidepressant response. • Prefrontal engagement differentially predicted response to SSRI and DBT treatment. • Examining prefrontal activity may allow for more individualized treatment in BPD. [ABSTRACT FROM AUTHOR]

Purpose: The study aims to analyze alterations in dynamic functional connectivity density (dFCD) and effective connectivity (dEC) patterns using functional magnetic resonance imaging (fMRI), hypothesizing that overactive bladder (OAB) patients will exhibit distinct dFCD and dEC patterns, reflecting altered neural communication underlying the OAB. Methods: Forty‐three female OAB patients and 40 female healthy controls (HC) underwent resting‐state fMRI. Sliding window correlation was used to calculate the variability of the dFCD. The changes in dFCD‐based dEC between the two groups were examined using Granger causal analysis. To describe the time‐varying Granger causality, a sliding‐window approach was utilized to divide time courses into a group of windows. We adopted a k‐means clustering method to cluster all matrices into discrete connectivity states. Results: Compared with HC, OAB females consistently had a dFCD (decreased) in the left anterior cingulate cortex (ACC) and left medial prefrontal cortex (mPFC) (p < 0.05, GRF corrected). In state 1, OAB patients had excitatory effective connections from bilateral ACC to left mPFC in comparison to HC. In state 2, there was an increase in dEC from the SMA to the mPFC. Participants with OAB showed significantly more inhibitory dorsolateral prefrontal cortex (dlPFC) connections between the left ACC and the right ACC in state 4, as well as an excitatory dEC connection between the right dlPFC and the left ACC in state 2 (p < 0.05, GRF corrected). Conclusion: OAB patients demonstrate significant alterations in dFCD and dEC patterns, which may be indicative of the neural mechanisms involved in OAB pathophysiology. [ABSTRACT FROM AUTHOR]

Objective: Spinal cord stimulation (SCS) is an invasive treatment option for patients suffering from chronic low-back pain (cLBP). It is an effective treatment that has been shown to reduce pain and increase the quality of life in patients. However, the activation of pain processing regions of cLBP patients receiving SCS has not been assessed using objective, quantitative functional imaging techniques. The purpose of the present study was to compare quantitative resting-state (rs)-fMRI and arterial spin labeling (ASL) measures between SCS patients and healthy controls and to correlate clinicalmeasures with quantitative multimodal imaging indices in pain regions. Methods: Multi-delay 3D GRASE pseudo-continuous ASL and rs-fMRI data were acquired from five patients post-SCS with cLBP and five healthy controls. Three ASL measures and four rs-fMRI measures were derived and normalized into MNI space and smoothed. Averaged values for each measure from a pain atlas were extracted and compared between patients and controls. Clinical pain scores assessing intensity, sensitization, and catastrophizing, as well as others assessing global pain effects (sleep quality, disability, anxiety, and depression), were obtained in patients and correlated with pain regions using linear regression analysis. Results: Arterial transit time derived from ASL and several rs-fMRI measures were significantly different in patients in regions involved with sensation (primary somatosensory cortex and ventral posterolateral thalamus [VPL]), pain input (posterior short gyrus of the insula [PS]), cognition (dorsolateral prefrontal cortex [DLPC] and posterior cingulate cortex [PCC]), and fear/stress response (hippocampus and hypothalamus). Unidimensional pain rating and sensitization scores were linearly associated with PS, VPL, DLPC, PCC, and/or amygdala activity in cLBP patients. Conclusion: The present results provide evidence that ASL and rs-fMRI can contrast functional activation in pain regions of cLBP patients receiving SCS and healthy subjects, and they can be associated with clinical pain evaluations as quantitative assessment tools. [ABSTRACT FROM AUTHOR]

Objective: The neurobiological mechanisms underpinning binge eating disorder (BED) in children remain largely unclear, as the alterations that have been identified to date may be attributable to BED, obesity, or compound effects. This study aimed to delineate functional connectivity (FC) patterns in inhibitory control and reward networks in preadolescent children with and without BED from the Adolescent Brain Cognitive Development (ABCD) Study according to BMI. Methods: Resting‐state FC was examined in the inhibitory control network by using seeds in the dorsolateral prefrontal cortex, the anterior cingulate cortex, and the posterior cingulate cortex, whereas the reward network included seeds in the orbitofrontal cortex, nucleus accumbens, and amygdala. Seed‐to‐voxel analyses characterized FC differences between preadolescent children with BED with a high BMI and those with BED with a low BMI. Results: We identified that BED was characterized by reduced connectivity between the reward network and regions in the default mode network, irrespective of weight status. Participants with BED also presented with hypoconnectivity in fronto‐amygdalar circuits, which has been consistently associated with impaired emotion regulation capacity. Conclusions: Our findings support that FC alterations between the reward network and the default mode network may be specifically impacted by the presence of BED as opposed to weight status. [ABSTRACT FROM AUTHOR]

Introduction: Recent resting-state electroencephalogram (EEG) studies have consistently reported an association between aberrant functional brain networks (FBNs) and treatment-resistant traits in patients with major depressive disorder (MDD). However, little is known about the changes in FBNs in response to external stimuli in these patients. This study investigates whether changes in the salience network (SN) could predict responsiveness to pharmacological treatment in resting-state and external stimuli conditions. Methods: Thirty-one drug-naïve patients with MDD (aged 46.61 ± 10.05, female 28) and twenty-one healthy controls (aged 43.86 ± 14.14, female 19) participated in the study. After 8 weeks of pharmacological treatment, the patients were divided into non-remitted MDD (nrMDD, n = 14) and remitted-MDD (rMDD, n = 17) groups. EEG data under three conditions (resting-state, standard, and deviant) were analyzed. The SN was constructed with three cortical regions as nodes and weighted phase-lag index as edges, across alpha, low-beta, high-beta, and gamma bands. A repeated measures analysis of the variance model was used to examine the group-by-condition interaction. Machine learning-based classification analyses were also conducted between the nrMDD and rMDD groups. Results: A notable group-by-condition interaction was observed in the highbeta band between nrMDD and rMDD. Specifically, patients with nrMDD exhibited hypoconnectivity between the dorsal anterior cingulate cortex and right insula (p = 0.030). The classification analysis yielded a maximum classification accuracy of 80.65%. Conclusion: Our study suggests that abnormal condition-dependent changes in the SN could serve as potential predictors of pharmacological treatment efficacy in patients with MDD. [ABSTRACT FROM AUTHOR]

We present a quantitative strategy to identify all projection neuron types from a given region with statistically different patterns of anatomical targeting. We first validate the technique with mouse primary motor cortex layer 6 data, yielding two clusters consistent with cortico-thalamic and intra-telencephalic neurons. We next analyze the presubiculum, a less-explored region, identifying five classes of projecting neurons with unique patterns of divergence, convergence, and specificity. We report several findings: individual classes target multiple subregions along defined functions; all hypothalamic regions are exclusively targeted by the same class also invading midbrain and agranular retrosplenial cortex; Cornu Ammonis receives input from a single class of presubicular axons also projecting to granular retrosplenial cortex; path distances from the presubiculum to the same targets differ significantly between classes, as do the path distances to distinct targets within most classes; the identified classes have highly non-uniform abundances; and presubicular somata are topographically segregated among classes. This study thus demonstrates that statistically distinct projections shed light on the functional organization of their circuit. The classification of different types of neurons has been a long-standing challenge in neuroscience. Here, the authors present a strategy to quantify all statistically distinct axonal patterns from a brain region based on their anatomical targeting, with this projection-driven neuron classification informing the functional architecture of the circuit. [ABSTRACT FROM AUTHOR]

Decision to explore new options with uncertain outcomes or exploit familiar options with known outcomes is a fundamental challenge that the brain faces in almost all real-life decisions. Previous studies have shown that humans use two main explorative strategies to negotiate this explore-exploit tradeoff. Exploring for the sake of information is called directed exploration, and exploration driven by behavioral variability is known as random exploration. While previous neuroimaging studies have shown different neural correlates for these explorative strategies, including right frontopolar cortex (FPC), right dorsolateral prefrontal cortex (DLPFC), and dorsal anterior cingulate cortex (dACC), there is still a lack of causal evidence for most of these brain regions. Here, we focused on the right DLPFC, which was previously supported to be involved in exploration. Using the continuous theta burst stimulation (cTBS) and Horizon task on twenty-five healthy right-handed adult participants, we showed that inhibiting rDLPFC did not change directed exploration but selectively reduced random exploration, by increasing reward sensitivity over the average reward of each option. This suggests a causal role for rDLPFC in random exploration, and further supports dissociable neural implementations for these two explorative strategies. [ABSTRACT FROM AUTHOR]

Introduction: Mental rotation (MR) tasks of body parts involve anatomically interconnected brain systems. The systems are implicated in sensorimotor information integration and activate cortical motor-related areas, corresponding to the execution of similar motor tasks. In this study, we aimed to investigate the effect of varying the angle in the hand MR task on cerebral activation of the motor-related areas. Methods: Twenty healthy right-handed participants were recruited. We investigated cerebral activation while each participant decided whether a hand-palm image, rotated by 0°, 90°, 180°, and 270°, was a right or left hand. Results and discussion: A significant negative correlation between the angle and brain activity was observed in the right and left supplementary motor area (SMA) and right posterior anterior cingulate gyrus. The SMA was inactivated with 180°- or 270°-rotated images in the regions of interest analysis. 180°- and 270°-rotated palms would be biomechanically difficult to position; thus, SMA deactivation may be closely associated with biomechanical constraints. This study provided novel findings regarding the neurophysiological mechanisms of motor imagery and may be useful in developing treatment plans using MR tasks during patient rehabilitation. [ABSTRACT FROM AUTHOR]

Mathematical algorithms known as "epigenetic clocks" use methylation values at a set of CpG sites to estimate the biological age of an individual in a tissue-specific manner. These clocks have demonstrated both acceleration and delays in epigenetic aging in multiple neuropsychiatric conditions, including schizophrenia and neurodevelopmental disorders such as autism spectrum disorder. However, no study to date has examined epigenetic aging in ADHD despite its status as one of the most prevalent neurodevelopmental conditions, with 1 in 9 children having ever received an ADHD diagnosis in the US. Only a handful of studies have examined epigenetic age in brain tissue from neurodevelopmental conditions, with none focused on ADHD, despite the obvious relevance to pathogenesis. Thus, here we asked if post-mortem brain tissue in those with lifetime histories of ADHD would show accelerated or delayed epigenetic age, as has been found for other neurodevelopmental conditions. We applied four different epigenetic clocks to estimate epigenetic age in individuals with ADHD and unaffected controls from cortical (anterior cingulate cortex, N = 55) and striatal (caudate, N = 56) post-mortem brain tissue, as well as peripheral blood (N = 84) and saliva (N = 112). After determining which epigenetic clock performed best in each tissue, we asked if ADHD was associated with altered biological aging in corticostriatal brain and peripheral tissues. We found that a range of epigenetic clocks accurately predicted chronological age in all tissues. We also found that a diagnosis of ADHD was not significantly associated with differential epigenetic aging, neither for the postmortem ACC or caudate, nor for peripheral tissues. These findings held when accounting for comorbid psychiatric diagnoses, substance use, and stimulant medication. Thus, in this study of epigenetic clocks in ADHD, we find no evidence of altered epigenetic aging in corticostriatal brain regions nor in peripheral tissue. We consider reasons for this unexpected finding, including the limited sampling of brain regions, the age range of individuals studied, and the possibility that processes that accelerate epigenetic age may be counteracted by the developmental delay posited in some models of ADHD. [ABSTRACT FROM AUTHOR]

Background: Sex differences in human brain anatomy have been well-documented, though remain significantly underexplored during early development. The neonatal period is a critical stage for brain development and can provide key insights into the role that prenatal and early postnatal factors play in shaping sex differences in the brain. Methods: Here, we assessed on-average sex differences in global and regional brain volumes in 514 newborns aged 0–28 days (236 birth-assigned females and 278 birth-assigned males) using data from the developing Human Connectome Project. We also assessed sex-by-age interactions to investigate sex differences in early postnatal brain development. Results: On average, males had significantly larger intracranial and total brain volumes, even after controlling for birth weight. After controlling for total brain volume, females showed significantly greater total cortical gray matter volumes, whilst males showed greater total white matter volumes. After controlling for total brain volume in regional comparisons, females had significantly increased white matter volumes in the corpus callosum and increased gray matter volumes in the bilateral parahippocampal gyri (posterior parts), left anterior cingulate gyrus, bilateral parietal lobes, and left caudate nucleus. Males had significantly increased gray matter volumes in the right medial and inferior temporal gyrus (posterior part) and right subthalamic nucleus. Effect sizes ranged from small for regional comparisons to large for global comparisons. Significant sex-by-age interactions were noted in the left anterior cingulate gyrus and left superior temporal gyrus (posterior parts). Conclusions: Our findings demonstrate that sex differences in brain structure are already present at birth and remain comparatively stable during early postnatal development, highlighting an important role of prenatal factors in shaping sex differences in the brain. Plain Language Summary: Sex differences in the human brain have attracted substantial scientific and societal interest, but less is known about whether the brain shows sex differences at birth. Studying sex differences at birth can help to understand how prenatal factors (e.g., hormone levels before birth) and early postnatal factors (e.g., exposure to the sensory environment and caregiver interactions) contribute to shaping sex differences in the brain. In this study, we investigated on-average sex differences in brain structure in a large sample of newborn infants shortly after birth. Our findings show that several on-average differences are present at birth, suggesting that factors before birth play an important role in initiating sex differences in the brain. Highlights: At birth, males on average show significantly increased total brain volumes compared to females even after accounting for sex differences in birth weight. After controlling for total brain volume, females on average show significantly increased total cortical gray matter volumes, while males show increased total white matter volumes. After controlling for total brain volume, significant on-average sex differences are observed in regions such as the corpus callosum (F > M), bilateral parietal lobes (F > M), left anterior cingulate gyrus (F > M), left caudate nucleus (F > M), and right medial and inferior temporal gyri (M > F). Fewer global and regional volumes showed significant sex-by-age interactions, except for the left anterior cingulate gyrus (F > M) and left superior temporal gyrus (M > F). Several sex differences that have previously been observed later in development are present from birth, emphasising the key role that prenatal factors play in initiating sex differences in the brain. [ABSTRACT FROM AUTHOR]

The insular cortex (IC) is a brain region that both receives relevant sensory information and is responsible for emotional and cognitive processes, allowing the perception of sensory information. The IC has connections with multiple sites of the pain matrix, including cortico-cortical interactions with the anterior cingulate cortex (ACC) and top-down connections with sites of descending pain inhibition. We explored the changes in the extracellular release of serotonin (5HT) and its major metabolite, 5-hydroxyindoleacetic acid (5HIAA), after inflammation was induced by carrageenan injection. Additionally, we explored the role of 5HT receptors (the 5HT1A, 5HT2A, and 5HT3 receptors) in the IC after inflammatory insult. The results showed an increase in the extracellular levels of 5HT and 5-HIAA during the inflammatory process compared to physiological levels. Additionally, the 5HT1A receptor was overexpressed. Finally, the 5HT1A, 5HT2A, and 5HT3 receptor blockade in the IC had antinociceptive effects. Our results highlight the role of serotonergic neurotransmission in long-lasting inflammatory nociception within the IC. [ABSTRACT FROM AUTHOR]

Different cortical systems to the hippocampus were activated using fMRI during different types of episodic memory task. For object with scene location episodic memory, the activations were high in cortical systems involved in spatial processing, including the ventromedial visual and medial parahippocampal system. These activations for the medial parahippocampal system were higher in the right hemisphere. The activations in the face and object processing ventrolateral visual cortical stream regions FFC, PIT, V8 and TE2p were higher in the object‐location in scene task than the reward‐location task, and were higher in the right hemisphere. For reward‐location in scene episodic memory, activations were also high in the ventromedial visual cortical spatial stream to the hippocampus, but were also selectively high in storage in key reward cortical regions (ventromedial prefrontal 10r, 10v, 10d; pregenual anterior cingulate d32, p24, p32, s32; and medial orbitofrontal cortex reward‐related pOFC, 11l, OFC). For word‐pair episodic memory, activations were lower in the ventromedial visual and medial parahippocampal spatial cortical stream, and were higher in language‐related regions in Broca's area (44, 45, 47l), and were higher in the left hemisphere for these regions and for the many highly connected inferior frontal gyrus regions in the left hemisphere. Further, effective connectivity analyses during the episodic memory tasks showed that the direction of connectivity for these systems was from early visual cortical regions V2–V4 to the ventromedial visual cortical regions VMV1–3 and VVC for spatial scene processing; was from the pregenual anterior cingulate and orbitofrontal cortex reward systems to the hippocampal system; and was from the FFC/V8/PIT system to TE2p in the visual inferior temporal visual cortex, which has connectivity to lateral parahippocampal TF, which in turn has forward effective connectivity to the hippocampus. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a neurodegenerative disorder that progressively involves brain regions with an often-predictable pattern. Damage to the brain appears to spread and worsen with time, but the molecular mechanisms underlying the region-specific distribution of AD pathology at different stages of the disease are still under-investigated. In this study, a whole-transcriptome analysis was carried out on brain samples from the hippocampus (HI), temporal and parietal cortices (TC and PC, respectively), cingulate cortex (CG), and substantia nigra (SN) of six subjects with a definite AD diagnosis and three healthy age-matched controls in duplicate. The transcriptomic results showed a greater number of differentially expressed genes (DEGs) in the TC (1571) and CG (1210) and a smaller number of DEGs in the HI (206), PC (109), and SN (60). Furthermore, the GSEA showed a difference between the group of brain areas affected early (HI and TC) and the group of areas that were subsequently involved (PC, CG, and SN). Notably, in the HI and TC, there was a significant downregulation of shared DEGs primarily involved in synaptic transmission, while in the PC, CG, and SN, there was a significant downregulation of genes primarily involved in protein folding and trafficking. The course of AD could follow a definite time- and severity-related pattern that arises from protein misfolding, as observed in the PC, CG, and SN, and leads to synaptic impairment, as observed in the HI and TC. Therefore, a map of the molecular and biological processes involved in AD pathogenesis may be traced. This could aid in the discovery of novel biological targets in order to develop effective and well-timed therapeutic approaches. [ABSTRACT FROM AUTHOR]

Objective Methods Results Significance Pathological amyloid‐β (Aβ) accumulation and hyperphosphorylated tau proteins have been described in resected temporal lobe specimens of epilepsy patients. We aimed to determine cerebrospinal fluid (CSF) Aβ1‐42 and p181‐tau levels and cerebral Aβ deposits on positron emission tomography (Aβ PET) and correlate these findings with cognitive performance in adults with drug‐resistant temporal lobe epilepsy (TLE).In this cross‐sectional study, we enrolled individuals with drug‐resistant TLE who were 25–55 years old. Each participant underwent 18F‐flutemetamol PET, determination of CSF Aβ1‐42, p181‐tau, and total tau, and a comprehensive neuropsychological assessment. We evaluated normalized standard uptake value ratios (SUVRs) for different brain regions on Aβ PET.Thirty patients (mean age = 41.9 ± SD 8.1 years, 57% men) were included. The median disease duration was 9.5 (interquartile range = 4–24) years. Twenty‐six patients (87%) had a clinically significant cognitive impairment on neuropsychological evaluation, 18 (69%) of the amnesic type. On Aβ PET, high uptake was observed in both mesial temporal regions (ipsilateral: SUVR z‐score = .90, 95% confidence interval [CI] = .60–1.20; contralateral: SUVR z‐score = .92, 95% CI = .57–1.27; p < .001), which was higher when compared to SUVR z‐scores in all the remaining regions (p < .001) and in the ipsilateral anterior cingulate (SUVR z‐score = .27, 95% CI = .04–.49, p = .020). No significant deposition was observed in other regions. Seven patients (23%) had low Aβ1‐42 levels, and two (7%) had elevated p181‐tau levels in CSF. Higher p181‐tau levels correlated with poorer verbal fluency (R = −.427, p = .044).Our findings reveal a considerable Aβ deposition in mesial temporal regions and ipsilateral anterior cingulate among adults with drug‐resistant TLE. Additionally, abnormal CSF Aβ1‐42 levels were observed in a significant proportion of patients, and p181‐tau levels were associated with verbal fluency. These results suggest that markers of neuronal damage can be observed in adults with TLE, warranting further investigation. [ABSTRACT FROM AUTHOR]

Schizophrenia (SCZ) and psychotic bipolar disorder (PBD) are two major psychotic disorders with similar symptoms and tight associations on the psychopathological level, posing a clinical challenge for their differentiation. This study aimed to investigate and compare the structural connectivity patterns of the limbic system between SCZ and PBD, and to identify specific regional disruptions associated with psychiatric symptoms. Using sMRI data from 146 SCZ, 160 PBD, and 145 healthy control (HC) participants, we employed a data-driven approach to segment the hippocampus, thalamus, hypothalamus, amygdala, and cingulate cortex into subregions. We then investigated the structural connectivity patterns between these subregions at the global and nodal levels. Additionally, we assessed psychotic symptoms by utilizing the subscales of the Brief Psychiatric Rating Scale (BPRS) to examine correlations between symptom severity and network metrics between groups. Patients with SCZ and PBD had decreased global efficiency (E glob) (SCZ: adjusted P <0.001; PBD: adjusted P = 0.003), local efficiency (E loc) (SCZ and PBD: adjusted P <0.001), and clustering coefficient (Cp) (SCZ and PBD: adjusted P <0.001), and increased path length (Lp) (SCZ: adjusted P <0.001; PBD: adjusted P = 0.004) compared to HC. Patients with SCZ showed more pronounced decreases in E glob (adjusted P <0.001), E loc (adjusted P <0.001), and Cp (adjusted P = 0.029), and increased Lp (adjusted P = 0.024) compared to patients with PBD. The most notable structural disruptions were observed in the hippocampus and thalamus, which correlated with different psychotic symptoms, respectively. This study provides evidence of distinct structural connectivity disruptions in the limbic system of patients with SCZ and PBD. These findings might contribute to our understanding of the neuropathological basis for distinguishing SCZ and PBD. • Schizophrenia and psychotic bipolar disorder show similar psychotic symptoms. • The study examined topological changes in the limbic system between schizophrenia and psychotic bipolar disorder. • Schizophrenia exhibited more severe global and nodal alterations. • Key subregions identified in the hippocampus, thalamus, and cingulate cortex. • The correlation between network and psychotic symptoms was reversed between the two disorders. [ABSTRACT FROM AUTHOR]

Inflammatory bowel diseases (IBD) are a group of chronic, non-specific intestinal diseases that could comorbid with varieties of negative emotional constructs, including pain-related negative emotions and trait negative emotions; however, the link between brain functions and different dimensions of negative emotions remains largely unknown. Ninety-eight patients with IBD and forty-six healthy subjects were scanned using a 3.0-T functional magnetic resonance imaging scanner. The amplitudes of low-frequency fluctuation (ALFF), regional homogeneity (ReHo), and degree centrality (DC) were used to assess resting-state brain activity. Partial least squares (PLS) correlation was employed to assess the relationship among abnormal brain activities, pain-related and trait negative emotions. Compared to controls, patients with IBD exhibited higher values of ALFF in the right anterior cingulate cortex (ACC), lower values of ALFF in the left postcentral gyrus, and higher values of DC in the bilateral ACC. Multivariate PLS correlation analysis revealed the brain scores of the ACC were correlated with pain-related negative emotions, the brain salience in the left postcentral gyrus was associated with the higher-order trait depression. These findings can enhance our comprehension of how pain-related negative emotion and trait negative emotion affect the brains of patients with IBD in distinct ways. [ABSTRACT FROM AUTHOR]

Film color and editing are crucial elements in filmmaking, posing significant questions about their effective use in eliciting emotional responses from viewers. While prior research has explored the impacts of color and editing independently, their combined effect remains largely unexplored, leaving the open question of how these elements together affect emotional perception. This study investigates the combined impact of film color and editing on emotion perception, utilizing both subjective behavioral scales and objective functional magnetic resonance imaging (fMRI) techniques. It employs two experiments with a two-factor design to assess the interactions between film color (colored and black-and-white) and film editing (fearful, neutral, and happy levels) on emotional perceptions. Under the direction of a professional filmmaker, a series of film sequences was created for six experimental conditions. In Experiment 1, 117 participants watched the film sequences and subjectively rated the emotional valence of the neutral face in the sequence, uncovering a significant interaction effect between film color and editing on the valence rating of the neutral face. In Experiment 2, 67 participants watched similar film sequences in an MRI scanner to analyze their brain activation patterns. Distinct activations were identified in regions including the insula, anterior cingulate cortices (ACC), and middle frontal gyrus, where a region-of-interest (ROI) analysis of the left ACC revealed an interaction effect on neural responses. These results underscore the integral role of color and editing in influencing viewers' emotion perception using two types of measurements. This research provides novel insights into the behavioral and neural responses to filmmaking elements that underpin film reception and offers practical implications for filmmakers, encouraging a more holistic approach to considering color and editing to further enrich the audience's emotional experiences at the pre-production stage of filmmaking. [ABSTRACT FROM AUTHOR]

Early life stress (ELS) yields cognitive impairments of unknown molecular and physiological origin. We found that fragmented maternal care of mice during a neonatal critical period from postnatal days P2–9 elevated dopamine receptor D2R and suppressed D4R expression, specifically within the anterior cingulate cortex (ACC) in only the male offspring. This was associated with poor performance on a two-choice visual attention task, which was acutely rescued in adulthood by local or systemic pharmacological rebalancing of D2R/D4R activity. Furthermore, ELS male mice demonstrated heightened hypothalamic orexin and persistently disrupted sleep. Given that acute sleep deprivation in normally reared male mice mimicked the ACC dopamine receptor subtype modulation and disrupted attention of ELS mice, sleep loss likely underlies cognitive deficits in ELS mice. Likewise, sleep impairment mediated the attention deficits associated with early adversity in human children, as demonstrated by path analysis on data collected with multiple questionnaires for a large child cohort. A deeper understanding of the sex-specific cognitive consequences of ELS thus has the potential to reveal therapeutic strategies for overcoming them. Editor's summary: Early life adversity (ELA) can have cognitive impacts that persist into adulthood, but the underlying brain mechanisms remain elusive. Here, Makino et al. show that fragmented maternal care led to cognitive dysfunction in adult male, but not female, mice. These findings were associated with disrupted sleep patterns and dysregulated dopamine receptor expression in the anterior cingulate cortex. Acute sleep disruption mimicked ELA-induced changes, and pharmacological rebalancing of DR signaling rescued cognitive dysfunction. Analysis of data from a cohort of young children showed that adversity negatively affected attention, and this relationship was mediated by poor sleep, indicating that the coupling of adversity, sleep, and attention is conserved across species. —Daniela Neuhofer [ABSTRACT FROM AUTHOR]

Expectations shape our perception, profoundly influencing how we interpret the world. Positive expectations about sensory stimuli can alleviate distress and reduce pain (e.g., placebo effect), while negative expectations may heighten anxiety and exacerbate pain (e.g., nocebo effect). To investigate the impact of the (an)hedonic aspect of expectations on subjective experiences, we measured neurobehavioral responses to the taste of hot sauce among participants with heterogeneous taste preferences. By identifying participants who "liked" versus those who strongly "disliked" spicy flavors and by providing contextual cues about the spiciness of the sauce to be tasted, we dissociated the effects of positive and negative expectations from sensory stimuli (i.e., visual and gustatory stimuli), which were the same across all participants. Our results indicate that positive expectations lead to modulations in the intensity of subjective experience. These modulations were accompanied by increased activity in brain regions previously linked to information integration and the placebo effect, including the anterior insula, dorsolateral prefrontal cortex, and dorsal anterior cingulate cortex, as well as a predefined "pleasure signature." In contrast, negative expectations decreased hedonic experience and increased neural activity in the previously validated "Neurological Pain Signature" network. These findings demonstrate that hedonic aspects of one's expectations asymmetrically shape how the brain processes sensory input and associated behavioral reports of one's subjective experiences of intensity, pleasure, and pain. Our results suggest a dissociable impact of hedonic information: positive expectations facilitate higher-level information integration and reward processing, while negative expectations prime lower-level nociceptive and affective processes. This study demonstrates the powerful role of hedonic expectations in shaping subjective reality and suggests potential avenues for consumer and therapeutic interventions targeting expectation-driven neural processes. Can positive and negative expectations of a sensory experience cause neuronal and perception differences? This study shows that sensory experiences and neuronal responses are shaped by whether a person likes spicy foods, suggesting that perception could be pharmacologically modulated. [ABSTRACT FROM AUTHOR]

High‐fat diet (HFD)‐induced obesity induces peripheral inflammation and hypothalamic pathogenesis linking the activation of astrocytes and microglia. Clinical evidence indicates a positive correlation between obesity and psychiatric disorders, such as depression. The connectivity of the frontal‐striatal (FS) circuit, involving the caudate putamen (CPu) and anterior cingulate cortex (ACC) within the prefrontal cortex (PFC), is known for its role in stress‐induced depression. Thus, there is a need for a thorough investigation into whether chronic obesity‐induced gliosis, characterized by the activation of astrocytes and microglia, in these brain regions of individuals with chronic obesity. The results revealed increased S100β+ astrocytes and Iba1+ microglia in the CPu and ACC of male obese mice, along with immune cell accumulation in meningeal lymphatic drainage. Activated GFAP+ astrocytes and Iba1+ microglia were observed in the corpus callosum of obese mice. Gliosis in the CPu and ACC was linked to elevated cleaved caspase‐3 levels, indicating potential neural cell death by chronic HFD feeding. There was a loss of myelin and adenomatous polyposis coli (APC)+ oligodendrocytes (OLs) in the corpus callosum, an area known to be linked with injury to the CPu. Additionally, reduced levels of aquaporin‐4 (AQP4), a protein associated within the glymphatic systems, were noted in the CPu and ACC, while ciliary neurotrophic factor (CNTF) gene expression was upregulated in these brain regions of obese mice. The in vitro study revealed that high‐dose CNTF causing a trend of reduced astrocytic AQP4 expression, but it significantly impaired OL maturation. This pathological evidence highlights that prolonged HFD consumption induces persistent FS gliosis and demyelination in the corpus callosum. An elevated level of CNTF appears to act as a potential regulator, leading to AQP4 downregulation in the FS areas and demyelination in the corpus callosum. This cascade of events might contribute to neural cell damage within these regions and disrupt the glymphatic flow. [ABSTRACT FROM AUTHOR]

Despite the prevalence of large-group living across the animal kingdom, no studies have examined the neural mechanisms that make group living possible. Spiny mice, Acomys , have evolved to live in large groups and exhibit a preference to affiliate with large over small groups. Here, we determine the neural circuitry that facilitates the drive to affiliate with large groups. We first identify an anterior cingulate cortex (ACC) to lateral septum (LS) circuit that is more responsive to large than small groups of novel same-sex peers. Using chemogenetics, we then demonstrate that this circuit is necessary for both male and female group investigation preferences but only males' preference to affiliate with larger peer groups. Furthermore, inhibition of the ACC-LS circuit specifically impairs social, but not nonsocial, affiliative grouping preferences. These findings reveal a key circuit for the regulation of mammalian peer group affiliation. • Spiny mice, but not C57BL/6J mice, exhibit affiliative-peer-group preferences • The ACC-LS circuit is necessary for group investigation preferences in spiny mice • Inhibition of the ACC-LS reverses affiliative group preferences in male spiny mice • The ACC-LS circuit does not modulate nonsocial group size preferences in spiny mice Fricker et al. demonstrate that the ACC-LS circuit is necessary for peer group size preferences in communally breeding male and female spiny mice. These findings show that the ACC-LS circuit is an integral mediator of peer group affiliation responses that are likely critical for the formation and possibly the cohesion of complex mammalian societies. [ABSTRACT FROM AUTHOR]

Irritable bowel syndrome (IBS) is a functional bowel disorder frequently associated with other pain syndromes and psychiatric conditions, including depression and anxiety. These abnormalities coincide with alterations in the brain's structure, particularly in the thalamus and cingulate system. Acupuncture has been demonstrated to be highly effective in treating IBS. However, it remains unclear how white matter (WM) tracts change after acupuncture treatment, and whether the neuroplasticity of these tracts can serve as a neural marker to assist in the development of novel treatments. In this study, we aim to answer these questions by investigating longitudinal changes in the WM of the thalamus and cingulate system in a group of diarrhea-predominant irritable bowel syndrome (IBS-D) patients before and after acupuncture treatment. We found that after acupuncture treatment, as IBS symptoms improved, there were significant changes in the microstructure of the right thalamus radiation (TR) (p<0.05) and the right cingulum hippocampus (CH) (p<0.05). At the same time, patients with reduced IBS symptom severity scores (SSSs) were associated with the change of the right CH (p=0.015, r=-0.491), while reduced depressive conditions correlated with the change of the left TR (p=0.019, r=0.418). In addition, the consequences for the quality of life (QOL) showed a correlation with the right cingulum [cingulate cortex (CC)] (p=0.012, r=0.504) and left TR (p=0.027, r=-0.397). Our study highlighted the potential implications of neuroplasticity in WM tracts for IBS. Furthermore, these findings suggested that the right CH, TR, and right CC can serve as potential "biomarkers" of IBS-D recovery under acupuncture treatments. [ABSTRACT FROM AUTHOR]

The processes involved in encoding and decoding signals in the human brain are a continually studied topic, as neuronal information flow involves complex nonlinear dynamics. This study examines awake human intracranial electroencephalography (iEEG) data from normal brain regions to explore how biological sex influences these dynamics. The iEEG data were analyzed using permutation entropy and statistical complexity in the time domain and power spectrum calculations in the frequency domain. The Bandt and Pompe method was used to assess time series causality by associating probability distributions based on ordinal patterns with the signals. Due to the invasive nature of data acquisition, the study encountered limitations such as small sample sizes and potential sources of error. Nevertheless, the high spatial resolution of iEEG allows detailed analysis and comparison of specific brain regions. The results reveal differences between sexes in brain regions, observed through power spectrum, entropy, and complexity analyses. Significant differences were found in the left supramarginal gyrus, posterior cingulate, supplementary motor cortex, middle temporal gyrus, and right superior temporal gyrus. This study emphasizes the importance of considering sex as a biological variable in brain dynamics research, which is essential for improving the diagnosis and treatment of neurological and psychiatric disorders. [ABSTRACT FROM AUTHOR]

Background: Epilepsy, a complex neurological disorder, is closely linked with structural and functional irregularities in the brain. However, the causal relationship between brain imaging‐derived phenotypes (IDPs) and epilepsy remains unclear. This study aimed to investigate this relationship by employing a two‐sample bidirectional Mendelian randomization (MR) approach. Methods: The analysis involved 3935 cerebral IDPs from the UK Biobank and all documented cases of epilepsy (all epilepsies) cohorts from the International League Against Epilepsy, with further validation through replication and meta‐analyses using epilepsy Genome‐Wide Association Studies datasets from the FinnGen database. Additionally, a multivariate MR analysis framework was utilized to assess the direct impact of IDPs on all epilepsies. Furthermore, we performed a bidirectional MR analysis to investigate the relationship between the IDPs identified in all epilepsies and the 15 specific subtypes of epilepsy. Results: The study identified significant causal links between four IDPs and epilepsy risk. Decreased fractional anisotropy in the left inferior longitudinal fasciculus was associated with a higher risk of epilepsy (odds ratio [OR]: 0.89, p = 3.31×10−5). Conversely, increased mean L1 in the left posterior thalamic radiation (PTR) was independently associated with a heightened epilepsy risk (OR: 1.14, p = 4.72×10−5). Elevated L3 in the left cingulate gyrus was also linked to an increased risk (OR: 1.09, p =.03), while decreased intracellular volume fraction in the corpus callosum was correlated with higher epilepsy risk (OR: 0.94, p = 1.15×10−4). Subtype analysis revealed that three of these IDPs are primarily associated with focal epilepsy (FE). Notably, increased L1 in the left PTR was linked to an elevated risk of hippocampal sclerosis (HS) and lesion‐negative FE, whereas elevated L3 in the left cingulate gyrus was associated with HS‐related FE. Conclusions: Our research offers genetic evidence for a causal link between brain IDPs and epilepsy. These results enhance our understanding of the structural brain changes associated with the onset and progression of epilepsy. [ABSTRACT FROM AUTHOR]

Simple Summary: Bipolar disorder is a psychiatric condition in which one prominent symptom is the regular occurrence of mood swings. Its root cause remains unclear; thus, this study was intended to provide new insights to better understand the genetics underlying such a disorder. Using samples obtained from three regions in the brain, it was found that some molecular and cellular mechanisms are involved in the disruption of neurobiological processes. The dysregulated expression of certain genes eventually leads to neurogenesis and neurotransmission impairment events in humans. Furthermore, these genes significant in the onset of bipolar disorder were identified and evaluated for the presence of variants, which may be targeted to engineer better curative treatment strategies for the disorder. Bipolar disorder (BPD) is a serious psychiatric condition that is characterized by the frequent shifting of mood patterns, ranging from manic to depressive episodes. Although there are already treatment strategies that aim at regulating the manifestations of this disorder, its etiology remains unclear and continues to be a question of interest within the scientific community. The development of RNA sequencing techniques has provided newer and better approaches to studying disorders at the transcriptomic level. Hence, using RNA-seq data, we employed intramodular connectivity analysis and network pharmacology assessment of disease-associated variants to elucidate the biological pathways underlying the complex nature of BPD. This study was intended to characterize the expression profiles obtained from three regions in the brain, which are the nucleus accumbens (nAcc), the anterior cingulate cortex (AnCg), and the dorsolateral prefrontal cortex (DLPFC), provide insights into the specific roles of these regions in the onset of the disorder, and present potential targets for drug design and development. The nAcc was found to be highly associated with genes responsible for the deregulated transcription of neurotransmitters, while the DLPFC was greatly correlated with genes involved in the impairment of components crucial in neurotransmission. The AnCg did show association with some of the expressions, but the relationship was not as strong as the other two regions. Furthermore, disease-associated variants or single nucleotide polymorphisms (SNPs) were identified among the significant genes in BPD, which suggests the genetic interrelatedness of such a disorder and other mental illnesses. DRD2, GFRA2, and DCBLD1 were the genes with disease-associated variants expressed in the nAcc; ST8SIA2 and ADAMTS16 were the genes with disease-associated variants expressed in the AnCg; and FOXO3, ITGA9, CUBN, PLCB4, and RORB were the genes with disease-associated variants expressed in the DLPFC. Aside from unraveling the molecular and cellular mechanisms behind the expression of BPD, this investigation was envisioned to propose a new research pipeline in studying the transcriptome of psychiatric disorders to support and improve existing studies. [ABSTRACT FROM AUTHOR]

Objective: Chronic kidney disease (CKD) is increasingly recognized as a risk factor for alterations in brain function. However, detecting early‐stage symptoms and structural changes remains challenging, potentially leading to delayed treatment. In our study, we aimed to investigate spontaneous brain activity changes in CKD patients using resting‐state functional magnetic resonance imaging (fMRI). Additionally, we explored the correlation between common biomarkers reflecting CKD severity and brain activity. Methods: We recruited a cohort of 22 non–dialysis‐dependent CKD patients and 22 controls for resting‐state fMRI scans. Amplitude of low‐frequency fluctuations (ALFFs) and regional homogeneity (ReHo) were calculated to evaluate brain activity. Regression analysis was conducted to explore the correlations between biomarkers reflecting the severity of CKD and brain activity. Results: CKD patients exhibited reduced z‐scored ALFF (zALFF) and mean ALFF (mALFF) in the bilateral putamen, right caudate nucleus, left anterior cingulate, and right precuneus. Changes in bilateral putamen were also found in smCohe‐ReHo and szCohe‐ReHo analyses. Urine albumin‐to‐creatinine ratio (UACR), urine protein‐to‐creatinine ratio (UPCR), and serum albumin levels were associated with attenuated putamen activity. Conclusion: Non–dialysis‐dependent CKD patients had changes in zALFF, mALFF, smCohe‐ReHo, and szCohe‐ReHo values in specific brain regions, especially bilateral putamen. UACR, UPCR, and serum albumin levels are associated with putamen activity attenuation in rs‐fMRI. [ABSTRACT FROM AUTHOR]

Background: The surgical treatment of brain tumors has developed over time, offering customized strategies for patients and their specific lesions. One of the most recent advances in pediatric neuro-oncological surgery is laser interstitial thermal therapy (LITT). However, its effectiveness and indications are still being evaluated. The aim of this work is to review the current literature on LITT for pediatric low-grade gliomas (pLGG) and evaluate our initial results in this context. Methods: We retrospectively reviewed our pediatric neurosurgery database for patients who received LITT treatment between November 2019 and December 2023. We collected data on the indications for LITT, technical issues during the procedure, and clinical and radiological follow-up. Results: Three patients underwent 5 LITT procedures for pLGG. The lesion was thalamo-peduncular in one patient, cingulate in one, and deep parietal in one patient. Two patients had a previous open resection done and were diagnosed with pLGG. One patient underwent a stereotaxic biopsy during the LITT procedure that was non-diagnostic. The same patient underwent a later open resection of the tumor in the cingulate gyrus. There were no surgical complications and all patients were discharged home on the first post-operative day. The follow-up period was between 20 and 40 months. Radiological follow-up showed a progressive reduction of the tumor in patients with LGG. Conclusion: Laser interstitial thermal therapy is a minimally invasive treatment that shows promise in treating deep-seated pLGG in children. The treatment has demonstrated a reduction in tumor volume, and the positive results continue over time. LITT can be used as an alternative treatment for tumors located in areas that are difficult to access surgically or in cases where other standard treatment options have failed. [ABSTRACT FROM AUTHOR]

Sensory integration is the province of the parietal lobe. The non-dominant hemisphere is responsible for both body sides, while the dominant hemisphere is responsible for the contralateral hemi-body. Furthermore, the posterior cingulate cortex (PCC) participates in a network involved in spatial orientation, attention, and spatial and episodic memory. Laser interstitial thermotherapy (LiTT) is a minimally invasive surgery for focal drug-resistant epilepsy (DRE) that can target deeper brain regions, and thus, region-specific symptoms can emerge. Here, we present an 18-year-old right-handed male with focal DRE who experienced seizures characterized by sensations of déjà vu, staring spells, and language disruption. A comprehensive evaluation localized the seizure focus and revealed a probable focal cortical dysplasia (FCD) in the left posterior cingulate gyrus. The patient underwent uneventful LiTT of the identified lesion. Post-operatively, he developed transient ipsilateral spatial neglect and contralateral sensory loss, as well as acalculia. His sensory symptoms gradually improved after the surgery, and he remained seizure-free after the intervention for at least 10 months (until the time of this writing). This rare case of ipsilateral spatial and visual hemineglect post-LiTT in epilepsy underscores the importance of recognizing atypical neurosurgical outcomes and considering individual variations in brain anatomy and function. Understanding the dynamics of cortical connectivity and handedness, particularly in pediatric epilepsy, may be crucial in anticipating and managing neurocognitive effects following epilepsy surgery. [ABSTRACT FROM AUTHOR]

Summary: This study aimed to reveal the pathophysiology of isolated rapid eye movement sleep behaviour disorder (RBD) in patients using multilayer network analysis. Participants eligible for isolated RBD were included and verified via polysomnography. Both iRBD patients and healthy controls underwent brain MRI, including T1‐weighted imaging and diffusion tensor imaging. Grey matter matrix was derived from T1‐weighted images using a morphometric similarity network. White matter matrix was formed from diffusion tensor imaging‐based structural connectivity. Multilayer network analysis of grey and white matter was performed using graph theory. We studied 29 isolated RBD patients and 30 healthy controls. Patients exhibited a higher average overlap degree (27.921 vs. 23.734, p = 0.002) and average multilayer clustering coefficient (0.474 vs. 0.413, p = 0.002) compared with controls. Additionally, several regions showed significant differences in the degree of overlap and multilayer clustering coefficient between patients with isolated RBD and healthy controls at the nodal level. The degree of overlap in the left medial orbitofrontal, left posterior cingulate, and right paracentral nodes and the multilayer clustering coefficients in the left lateral occipital, left rostral middle frontal, right fusiform, right inferior posterior parietal, and right parahippocampal nodes were higher in patients with isolated RBD than in healthy controls. We found alterations in the multilayer network at the global and nodal levels in patients with isolated RBD, and these changes may be associated with the pathophysiology of isolated RBD. Multilayer network analysis can be used widely to explore the mechanisms underlying various neurological disorders. [ABSTRACT FROM AUTHOR]