Brain Regions Research Articles

Neurocognitive correlates of cerebral mitochondrial function and energy metabolism using phosphorus magnetic resonance spectroscopy in older adults.

The goal of the current study was to learn about the role of cerebral mitochondrial function on cognition. Based on established cognitive neuroscience, clinical neuropsychology, and cognitive aging literature, we hypothesized mitochondrial function within a focal brain region would map onto cognitive behaviors linked to that brain region. To test this hypothesis, we used phosphorous (31P) magnetic resonance spectroscopy (MRS) to derive indirect markers of mitochondrial function and energy metabolism across two regions of the brain (bifrontal, left temporal). We administered cognitive tasks sensitive to frontal-executive or temporal-hippocampal systems to a sample of 70 cognitively unimpaired older adults with subjective memory complaints and a first-degree family history of Alzheimer's disease and predicted better executive function and recent memory performance would be related to greater frontal and temporal 31P MRS indirect markers, respectively. Results of separate hierarchical linear regressions indicated better recent memory scores were related to 31P MRS indirect markers of lower static energy and higher energy reserve within the left temporal voxel; these findings were associated with moderate effect sizes. Contrary to predictions, executive function performance was unrelated to 31P MRS indirect markers within the bilateral frontal voxel, which may reflect a combination of theoretical and/or methodological issues. Findings represent a snapshot of the relationship between cognition and 31P MRS indirect markers of mitochondrial function, providing potential avenues for future work investigating mitochondrial underpinnings of cognition. 31P MRS may provide a sensitive neuroimaging marker for differences in aspects of memory among persons at-risk for mild cognitive impairment or dementia.

Alterations of regional homogeneity and functional connectivity in different hoehn and yahr stages of Parkinson's disease

PurposeUsing regional homogeneity (ReHo) and functional connectivity (FC) to assess alterations in brain function and their potential relation to different Hoehn and Yahr (H&Y) stages in Parkinson's disease (PD). Materials and methods66 patients with PD and 57 age- and sex-matched healthy control (HC) participants were recruited. All subjects underwent clinical assessments and resting-state functional magnetic resonance imaging (rs-fMRI) scanning. We analyzed alterations in regional brain activity using ReHo analyses in all subjects and further explored their relationship to disease severity. Finally, the brain region significantly associated with disease severity was used as a seed point to analyze the FC changes between it and other brain regions in the whole brain. ResultsCompared with HC participants, PD patients showed a significant decrease ReHo in the sensorimotor network (bilateral precentral and postcentral gyrus). The ReHo value of the left precentral gyrus in PD patients decreased with increasing H&Y stage and correlated negatively with Unified Parkinson’s Disease Rating Scale (UPDRS) III scores. Further, FC analysis of the left precentral gyrus as a region of interest showed that functional activity between the left precentral gyrus and sensorimotor network, default network, and visual network was decreased. ConclusionThe left precentral gyrus plays an important role in the pathophysiological mechanisms of PD patients, and this finding further highlights the potential of the primary motor cortex (M1) as a non-invasive therapeutic target for neuromodulation in PD patients.

Effects of robot-assisted hand function therapy on brain functional mechanisms: a synchronized study using fNIRS and sEMG

BackgroundRobot-assisted hand function therapy is pivotal in the rehabilitation of patients with stroke; however, its therapeutic mechanism remains elusive. Currently, research examining the impact of robot-assisted hand function therapy on brain function in patients with stroke is scarce, and there is a lack of studies investigating the correlation between muscle activity and alterations in brain function.ObjectiveThis study aimed to investigate the correlation between forearm muscle movement and brain functional activation by employing the synchronized use of functional near-infrared spectroscopy and surface electromyography methods. Moreover, it sought to compare neural activity patterns during different rehabilitation tasks and refine the mechanism of robot-assisted hand function therapy for post-stroke hand function impairments.MethodsStroke patients with hand dysfunction underwent three sessions of robot-assisted hand function therapy within 2 weeks to 3 months of onset. The fNIRS-sEMG synchronous technique was used to observe brain function and forearm muscle activation. Ten participants were randomly assigned to receive mirror, resistance, or passive rehabilitation training. During the intervention, cortical and muscle activation information was obtained using fNIRS and electromyographic signals. The primary outcomes included changes in oxyhemoglobin concentration and root mean square of surface electromyography.ResultsCompared to the resting state, the Oxy-Hb concentration in the brain regions involved in three rehabilitation tasks with robot-assisted hand function therapy significantly increased (p < 0.05). Mirror therapy significantly enhanced the prefrontal cortex and the superior frontal cortex activation levels. In contrast, resistance therapy significantly promoted the activation of the supplementary motor area and the premotor cortex. Passive rehabilitation tasks showed some activation in the target brain area premotor cortex region. Robot-assisted hand function therapy has shown that forearm muscle movement is closely related to oxygenated hemoglobin concentration activity in specific brain regions during different rehabilitation tasks.ConclusionThe simultaneous sEMG-fNIRS study found a significant correlation between muscle movement and brain activity after stroke, which provides an important basis for understanding the treatment mechanism of hand function impairment.

Olfactory and trigeminal routes of HSV-1 CNS infection with regional microglial heterogeneity.

Herpes simplex virus type 1 (HSV-1) primarily targets the oral and nasal epithelia before establishing latency in the trigeminal ganglion (TG) and other peripheral ganglia. HSV-1 can also infect and become latent in the central nervous system (CNS) independent of latency in the TGs. Recent studies suggest entry to the CNS via two distinct routes: the TG-brainstem connection and olfactory nerve; however, to date, there is no characterization of brain regions targeted during HSV-1 primary infection. Furthermore, the immune response by microglia may also contribute to the heterogeneity between different brain regions. However, the response to HSV-1 by microglia has not been characterized in a region-specific manner. This study investigated the time course of HSV-1 spread within the olfactory epithelium (OE) and CNS following intranasal inoculation and the corresponding macrophage/microglial response in a C57BL/6 mouse model. We found an apical to basal spread of HSV-1 within the OE and underlying tissue accompanied by an inflammatory response of macrophages. OE infection was followed by infection of a small subset of brain regions targeted by the TG in the brainstem and other cranial nerve nuclei, including the vagus and hypoglossal nerve. Furthermore, other brain regions were positive for HSV-1 antigens, such as the locus coeruleus (LC), raphe nucleus (RaN), and hypothalamus while sparing the hippocampus and cortex. Within each brain region, microglia activation also varied widely. These findings provide critical insights into the region-specific dissemination of HSV-1 within the CNS, elucidating potential mechanisms linking viral infection to neurological and neurodegenerative diseases.IMPORTANCEThis study shows how herpes simplex virus type 1 (HSV-1) spreads within the brain after infecting the nasal passages. Our data reveal the distinct pattern of HSV-1 through the brain during a non-encephalitic infection. Furthermore, microglial activation was also temporally and spatially specific, with some regions of the brain having sustained microglial activation even in the absence of viral antigens. Previous reports have identified specific brain regions found to be positive for HSV-1 infection; however, to date, there has not been a concise investigation of the anatomical spread of HSV-1 and the brain regions consistently vulnerable to viral entry and spread. Understanding these region-specific differences in infection and immune response is crucial because it links HSV-1 infection to potential triggers for neurological and neurodegenerative diseases.

Abnormal Granger causal connectivity based on altered gray matter volume and associated neurotransmitters of adolescents with internet gaming disorder revealed by a multimodal neuroimaging study

Although prior studies have revealed alterations in gray matter volume (GMV) among individuals with internet gaming disorder (IGD). The brain's multifaceted functions hinge crucially on the intricate connections and communication among distinct regions. However, the intricate interaction of information between brain regions with altered GMV and other regions, and how they synchronize with various neurotransmitter systems, remains enigmatic. Therefore, we aimed to integrate structural, functional and molecular data to explore the GMV-based Granger causal connectivity abnormalities and their correlated neurotransmitter systems in IGD adolescents. Voxel-based morphometry (VBM) analysis was firstly performed to investigate GMV differences between 37 IGD adolescents and 35 matched controls. Brain regions with altered GMV were selected as seeds for further Granger causality analysis (GCA). Two-sample t tests were performed using the SPM12 toolkit to compare the GMV and Granger causal connectivity between IGD and control groups (GRF corrected, Pvoxel<0.005, Pcluster<0.05). Then, GMV-based Granger causal connectivity was spatially correlated with PET- and SPECT-derived maps covering multifarious neurotransmitter systems. Multiple comparison correction was performed using false discovery rate (FDR). Compared with controls, IGD adolescents showed higher GMV in the caudate nucleus and lingual gyrus. For the GCA, IGD adolescents showed higher Granger causal connectivity from insula, putamen, supplementary motor area (SMA) and middle cingulum cortex (MCC) to the caudate nucleus, and lower Granger causal connectivity from superior/inferior parietal gyrus (SPG/IPG) and middle occipital gyrus (MOG) to the lingual gyrus. Besides, GMV-based Granger causal connectivity of IGD adolescents were associated with the dopaminergic, serotonergic, GABAergic and noradrenaline systems. This study revealed that the caudate nucleus and lingual gyrus may be the key sites of neuroanatomical changes in IGD adolescents, and whole-brain Granger causal connectivity abnormalities based on altered GMV involved large brain networks including reward, cognitive control, and visual attention networks, and these abnormalities are associated with a variety of neurotransmitter systems, which may be associated with higher reward sensitivity, cognitive control, and attention control dysfunction.

Transcranial Focused Ultrasound Neuromodulation in Psychiatry: Main Characteristics, Current Evidence, and Future Directions

Non-invasive brain stimulation (NIBS) techniques are designed to precisely and selectively target specific brain regions, thus enabling focused modulation of neural activity. Among NIBS technologies, low-intensity transcranial focused ultrasound (tFUS) has emerged as a promising new modality. The application of tFUS can safely and non-invasively stimulate deep brain structures with millimetric precision, offering distinct advantages in terms of accessibility to non-cortical regions over other NIBS methods. However, to date, several tFUS aspects still need to be characterized; furthermore, there are only a handful of studies that have utilized tFUS in psychiatric populations. This narrative review provides an up-to-date overview of key aspects of this NIBS technique, including the main components of a tFUS system, the neuronavigational tools used to precisely target deep brain regions, the simulations utilized to optimize the stimulation parameters and delivery of tFUS, and the experimental protocols employed to evaluate the efficacy of tFUS in psychiatric disorders. The main findings from studies in psychiatric populations are presented and discussed, and future directions are highlighted.

Maternal separation alters peripheral immune responses associated with IFN-γ and OT in mice

The co-evolution of social behavior and the immune system plays a critical role in individuals' adaptation to their environment. However, also need for further research on the key molecules that co-regulate social behavior and immunity. This study focused on neonatal mice that were separated from their mothers for 4 hours per day between the 6th and 16th day after birth. The results showed that these mice had lower plasma levels of IFN-γ and oxytocin, but higher levels of plasma glucocorticoids (GC), then impacting their social abilities. Additionally, maternal separation led to decreased levels of BDNF, IGF2, and CREB mRNAs in the hippocampus, while levels in the prefrontal cortex (PFC) remained unaffected. Maternal separation also resulted in increased levels of oxytocin and CRH mRNA in the hypothalamus, as well as an increase in CD45+ lymphocyte subsets in the meninges and choroid plexus (CP), with CD8+ lymphocytes in meninges and CD4+ lymphocytes in CP showing an increase. In IFN-γ-/- mice, a decrease in social preference was observed alongside lower plasma oxytocin levels. Moreover, IFN-γ-/- mice exhibited reduced numbers of oxytocin neurons in the paraventricular nucleus of the paraventricular nucleus of hypothalamus (PVN), decreased BDNF levels in the PFC and hippocampus, and alterations in CD45+ lymphocytes in CP and meninges, with an increase in CD8+ lymphocytes in meninges and CD4+ lymphocytes in CP. These findings highlight the immunological impact of social stress on IFN-γ regulation, suggesting that the immunomodulatory molecule IFN-γ may influence social behavior by affecting synaptic efficiency in brain regions such as the hippocampus and PFC, which are linked to oxytocin in the PVN.

A Relationship of Monoamine Oxidase-A with Serotonin in Violent Antisocial Behavior in Iraqi Prisoners

It is thought that the monoamine oxidase-A (MAOA) enzyme, which catalyzes key brain signaling chemicals like serotonin, noradrenaline, and dopamine, indirectly influences antisocial behavior by disrupting the neurotransmitter balance in brain regions and neural networks. This study aims to assess the MAOA enzyme level in serum and serotonin linked to antisocial behavior in cases in the prison of Baghdad City, Iraq. Blood samples were collected from (63) prisoners and (27) control groups, ages 18 years to 65 years, with a mean ± SD of 37.8 ± 8.8, all males, with different prison terms and different crimes for prisoners in the prison at Baghdad City, Iraq. MAOA and serotonin levels were measured in serum in prisoners and healthy men, and the results showed the serum levels of MAOA enzyme and serotonin were decreased in prisoners compared to the healthy (11.5 IU/ml vs. 19.5 IU/ml) and (79 IU/ml vs. 439 IU/ml), respectively, with the observed difference being significant (P &lt; 0.001(. The results of the relationship between education and social violence were: illiterate 11.1%, primary school 27%, secondary 52.4%, and university 9.5%. The median serum level of MAOA and serotonin in the age group 18–39 years was (11.3 IU/ml, 68.3 ng/ml), respectively, and in the age group 40–65 years was (13 IU/ml, 139 ng/ml), respectively.

The causal relationship of DTI phenotypes and epilepsy: A two sample mendelian randomization study.

Clinical studies indicated a link between DTI imaging characteristics and epilepsy, but the causality of this connection had not been established. Therefore, we employed the Mendelian randomization analysis method to determine the causal relationship between DTI imaging characteristics and epilepsy. We used Mendelian randomization analysis to identify the causal relationship between brain structure and the risk of epilepsy. GWAS data of DTI phenotypes, focal epilepsy, and genetic generalized epilepsy (GGE) were utilized in the analysis. Our study found that DTI imaging phenotypes had a causal risk relationship with epilepsy. These phenotypes had a statistical impact on the risk of epilepsy seizures. There were differences in DTI phenotype causality between GGE and focal epilepsy, which were associated with the clinical phenotype differences of the two types of epilepsy. Our study demonstrated that the diagnosis of subtypes could be assisted by comparing the differences in DTI phenotypes of specific brain regions. This meant that by studying the changes in brain regions before the onset of epilepsy, we might be able to intervene in epilepsy at an earlier stage. Our study used Mendelian randomization to explore the causal relationship between brain structure, as seen in DTI imaging, and epilepsy. We found that specific DTI phenotypes are linked to an increased risk of epilepsy seizures, with notable differences between genetic generalized epilepsy and focal epilepsy. This suggested that analyzing DTI phenotypes could help in diagnosing and potentially intervening in epilepsy earlier by finding brain changes before seizures begin.

Behavioral and psychological symptoms and brain volumes in community-dwelling older persons from the Nakayama Study

The frequency of behavioral and psychological symptoms of dementia (BPSD) is high, and it is a challenge to elucidate its neural substrates underlying their development. In recent years, many findings have been reported on the relationship between BPSD and brain volume in dementia patients. However, the results are not fully conclusive. Furthermore, there have been few population-based studies. Therefore, the relationship between BPSD and brain volume was investigated as an exploratory study. Of the 927 older persons who participated in the fifth Nakayama study, 90 were included in this analysis, consisting of 52 patients with mild cognitive impairment and 38 patients with dementia, with head MRI and the Neuropsychiatric Inventory (NPI) data. Multiple regression analysis was used to examine the association between the total score of each BPSD score on the NPI and brain volume estimated by FreeSurfer. On multivariate adjustment, even after false discovery rate correction, insular cortical volumes decreased significantly as total scores for apathy/indifference increased (p value = 0.002, q-value = 0.01). Similarly, total brain volume decreased significantly as total scores for appetite and eating disturbance increased (p value = 0.03), and parietal, temporal, and hippocampal cortical volumes also decreased significantly as total scores for appetite and eating disturbance increased (all p and q values < 0.05). This study’s results suggest that apathy is negatively correlated with insular cortical volume, and that appetite and eating disturbance are also correlated with brain regions, including parietal, temporal, and hippocampal volume in a community-dwelling older population.

White matter integrity and motor function: a link between cerebral myelination and longitudinal changes in gait speed in aging.

Gait speed is a robust health biomarker in older adults, correlating with the risk of physical and cognitive impairments, including dementia. Myelination plays a crucial role in neurotransmission and consequently affects various functions, yet the connection between myelination and motor functions such as gait speed is not well understood. Understanding this link could offer insights into diagnosing and treating neurodegenerative diseases that impair mobility. This study analyzed 437 longitudinal observations from 138 cognitively unimpaired adults, aged 22 to 94years, to investigate the relationship between myelin content and changes in gait speed over an average of 6.42years. Myelin content was quantified using a novel multicomponent magnetic resonance relaxometry method, and both usual and rapid gait speeds (UGS, RGS) were measured following standard protocols. Adjusting for covariates, we found a significant fixed effect of myelin content on UGS and RGS. Longitudinally, lower myelin content was linked to a greater decline in UGS, particularly in brain regions associated with motor planning. These results suggest that changes in UGS may serve as a reliable marker of neurodegeneration, particularly in cognitively unimpaired adults. Interestingly, the relationship between myelin content and changes in RGS was only observed in a limited number of brain regions, although the reason for such local susceptibility remains unknown. These findings enhance our understanding of the critical role of myelination in gait performance in unimpaired adults and provide evidence of the interconnection between myelin content and motor functionimpairment.

Cortico-thalamic communication for action coordination in a skilled motor sequence.

The coordination of forelimb and orofacial movements to compose an ethological reach-to-consume behavior likely involves neural communication across brain regions. Leveraging wide-field imaging and photo-inhibition to survey across the cortex, we identified a cortical network and a high-order motor area (MOs-c), which coordinate action progression in a mouse reach-and-withdraw-to-drink (RWD) behavior. Electrophysiology and photo-inhibition across multiple projection neuron types within the MOs-c revealed differential contributions of pyramidal tract and corticothalamic (CT MOs ) output channels to action progression and hand-mouth coordination. Notably, CT MOs display sustained firing throughout RWD sequence and selectively enhance RWD-relevant activity in postsynaptic thalamus neurons, which also contribute to action coordination. CT MOs receive converging monosynaptic inputs from forelimb and orofacial sensorimotor areas and are reciprocally connected to thalamic neurons, which project back to the cortical network. Therefore, motor cortex corticothalamic channel may selectively amplify the thalamic integration of cortical and subcortical sensorimotor streams to coordinate a skilled motor sequence.

Multimodal MRI changes associated with non-motor symptoms of rapid eye movement sleep behaviour disorder in Parkinson's disease patients.

Parkinson's disease (PD), a prevalent neurodegenerative disorder, assumes a more adverse prognosis when accompanied by rapid eye movement sleep disorder (RBD). Non-motor symptoms, particularly sleep and emotional disturbances, significantly impair patients' quality of life. This study aimed to investigate the neuroimaging underpinnings of PD-RBD using structural and functional magnetic resonance imaging (MRI) and to explore the associations between these imaging biomarkers and non-motor symptoms. Brain scans were acquired from 33 PD patients without and 21 with probable RBD (PD-pRBD). Comparative analyses were performed to evaluate structural and functional alterations between the two groups. Additionally, the correlations between neuroimaging metrics and clinical assessment scales were assessed. PD-pRBD patients demonstrated more pronounced grey matter atrophy, particularly in the putamen and insula. Functional MRI revealed decreased amplitude of low-frequency fluctuations (ALFF) in the bilateral posterior cingulate cortex and left precuneus of PD-pRBD patients. Furthermore, reduced functional connectivity (FC) was observed in specific regions of the whole brain and within the default mode network (DMN) in PD-pRBD. Notably, a negative correlation was found between mean ALFF values in the left posterior cingulate cortex of PD-pRBD patients and Hamilton Depression Rating Scale scores. PD-pRBD is characterized by more severe grey matter loss and functional MRI abnormalities compared to PD alone. Dysfunction of the posterior cingulate cortex is implicated in more pronounced affective impairments, providing novel insights into the complex pathophysiology of PD-RBD.

Nitric oxide donors rescue metabolic and mitochondrial dysfunction in obese Alzheimer’s model

Reduced nitric oxide (NO) bioavailability is a pathological link between obesity and Alzheimer’s disease (AD). Obesity-associated metabolic and mitochondrial bioenergetic dysfunction are key drivers of AD pathology. The hypothalamus is a critical brain region during the development of obesity and dysfunction is an area implicated in the development of AD. NO is an essential mediator of blood flow and mitochondrial bioenergetic function, but the role of NO in obesity-AD is not entirely clear. We investigated diet-induced obesity in female APPswe/PS1dE9 (APP) mouse model of AD, which we treated with two different NO donors (sodium nitrite or L-citrulline). After 26 weeks of a high-fat diet, female APP mice had higher adiposity, insulin resistance, and mitochondrial dysfunction (hypothalamus) than non-transgenic littermate (wild type) controls. Treatment with either sodium nitrite or L-citrulline did not reduce adiposity but improved whole-body energy expenditure, substrate oxidation, and insulin sensitivity. Notably, both NO donors restored hypothalamic mitochondrial respiration in APP mice. Our findings suggest that NO is an essential mediator of whole-body metabolism and hypothalamic mitochondrial function, which are severely impacted by the dual insults of obesity and AD pathology.

Association between focal amyloid deposition and cognitive impairment in individuals below the amyloid threshold

PurposeThis study aimed to investigate the characteristics of individuals with amyloid levels below the threshold. To achieve this, we differentiated between two groups: those with global amyloid negativity but focal deposition [G(–)F(+)] and those without focal deposition [G(–)F(–)].Materials and methodsA total of 2,677 participants were diagnosed with cognitive unimpairment (CU) or mild cognitive impairment (MCI). MRI-based regional centiloid (CL) values were used to establish threshold values for each brain region. After applying a cutoff of 20 rdcCL to identify amyloid positivity, participants who were globally amyloid-negative were grouped into three categories: those who showed focal amyloid uptake [G(–)F(+)], individuals without focal amyloid deposition but with relatively high CL(HC) levels comparable to those in the focal uptake group [G(–)F(–) HC)], and those with relatively low CL(LC) levels [G(–)F(–) LC]. We compared the neuropsychological test results and brain structural changes between these groups using ANCOVA.ResultsThe G(–)F(+) group demonstrated a lower cortical thickness (P &amp;lt; 0.001) than the G(–)F(–) HC group. In neuropsychological tests, the G(–)F(+) group exhibited lower the Seoul Verbal Learning Test delayed recall (SVLT-DR) and Mini Mental State Examination (MMSE), and showed progressed clinical status in the clinical dementia rating–sum of boxes (CDR-SOB) compared to the G(–)F(–) HC group (P &amp;lt; 0.001). The subsequent sensitivity analyses confirmed the persistence of these findings.ConclusionsIndividuals with focal amyloid deposition [G(–)F(+)] exhibited higher rates of cognitive impairment compared to patients with similar levels of amyloid, underscoring the importance of monitoring the progression of focal uptake, even when it remains below the amyloid threshold.

Posterior Basolateral Amygdala is a Critical Amygdaloid Area for Temporal Lobe Epilepsy.

The amygdaloid complex consists of multiple nuclei and is a key node in controlling temporal lobe epilepsy (TLE) in both human and animal model studies. However, the specific nucleus in the amygdaloid complex and the neural circuitry governing seizures remain unknown. Here, it is discovered that activation of glutamatergic neurons in the posterior basolateral amygdala (pBLA) induces severe seizures and even mortality. The pBLA glutamatergic neurons project collateral connections to multiple brain regions, including the insular cortex (IC), bed nucleus of the stria terminalis (BNST), and central amygdala (CeA). Stimulation of pBLA-targeted IC neurons triggers seizures, whereas ablation of IC neurons suppresses seizures induced by activating pBLA glutamatergic neurons. GABAergic neurons in the BNST and CeA establish feedback inhibition on pBLA glutamatergic neurons. Deleting GABAergic neurons in the BNST or CeA leads to sporadic seizures, highlighting their role in balancing pBLA activity. Furthermore, pBLA neurons receive glutamatergic inputs from the ventral hippocampal CA1 (vCA1). Ablation of pBLA glutamatergic neurons mitigates both acute and chronic seizures in the intrahippocampal kainic acid-induced mouse model of TLE. Together, these findings identify the pBLA as a pivotal nucleus in the amygdaloid complex for regulating epileptic seizures in TLE.

Neurostructural features predict binge drinking in emerging adulthood: Evidence from a 5-year follow-up study

BackgroundBinge drinking (BD) involves consuming large amounts of alcohol within a short timeframe, leading to a blood alcohol concentration of 0.08g/dL or above. This pattern of alcohol consumption is prevalent among young adults and has significant implications for brain structure and subsequent drinking behaviors. MethodsIn this prospective longitudinal study, we employed zero-inflated negative binomial regression models to examine whether various neurostructural features (i.e., volume, surface area, cortical thickness) of brain regions involved in executive and emotional/motivational processes at the age of 18–19 could predict number of BD episodes five years later, at ages 23–24, once participants were expected to complete their university degree. Specifically, we recorded magnetic resonance imaging (MRI) data from 68 students who completed both the baseline MRI and follow-up alcohol use assessment, with the aim of analyzing the predictive value of these neurostructural characteristics five years later. ResultsThe analysis revealed that a larger surface area in the caudal division of the right middle frontal gyrus was significantly associated with a higher incidence rate of BD episodes (IRR = 2.24, 95 % CI = 1.28–3.91, p = 0.005). Conversely, a smaller surface area in the right caudal anterior cingulate cortex was associated with a higher incidence rate of BD episodes (IRR = 0.61, 95 % CI = 0.44–0.85, p = 0.004). ConclusionsThese findings suggest that specific neurostructural characteristics during adolescence can predict BD behaviors in young adulthood. This highlights the potential of neuroimaging to identify individuals at risk for developing problematic alcohol use.

Delayed Recovery After Exercise-Induced Pain in People with Chronic Widespread Muscle Pain Related to Cortical Connectivity

Background/Objectives: There is a subset of patients with pain who become worse after exercise. To explore this, we examined the responses of people with chronic primary pain to a standardized high intensity exercise protocol used to induce delayed onset muscle soreness (DOMS). Methods: Ten participants with a diagnosis of chronic widespread muscle pain (CWMP) were matched by age and reported gender to ten participants without muscle pain (i.e., no pain (NP)). Participants completed a standardized DOMS protocol. Pain intensity in the arm at rest and with movement was assessed using daily electronic diaries. Peak pain, the timing of peak pain, and the time to recovery were compared between groups. Associations of pain variables with the functional connectivity of the sensorimotor (SMN), cerebellum, frontoparietal control (FPN), and default mode network (DMN) both within network nodes and the rest of the brain was assessed. Results: Significant differences in peak pain, the time to peak pain, and the time to recovery were noted between groups for both pain at rest and pain with movement after controlling for catastrophizing and pain resilience. Connectivity across the SMN, FPN, and DMN was associated with all pain-related variables. Significant group differences were identified between groups. Conclusions: A standardized muscle “injury” protocol resulted in more pain, a longer time to peak pain, and a longer time to resolve pain in the patient group compared to the NP group. These differences were associated with differences in connectivity across brain regions related to sensorimotor integration and appraisal. These findings provide preliminary evidence of the dysregulation of responses to muscle (micro)trauma in people with chronic pain.

Transcranial Magnetic Stimulation in Schizophrenia Patients

In schizophrenia, while antipsychotic medications are the primary treatment, auditory hallucinations may sometimes persist despite pharmacotherapy, and negative symptoms and cognitive impairments often show a limited response to these medications. Transcranial magnetic stimulation (TMS) has emerged as a promising adjunctive treatment, capable of modulating neuronal activity in targeted brain regions. Low-frequency repetitive TMS (rTMS) directed at the left temporoparietal cortex has demonstrated efficacy in reducing auditory hallucinations. In addressing negative symptoms, high-frequency rTMS applied to the dorsolateral prefrontal cortex has shown some effectiveness, though outcomes can vary. Innovative techniques, including theta burst stimulation and personalized approaches utilizing neuroimaging, are currently under investigation to further enhance the therapeutic potential of TMS. This review examines the application of TMS in the treatment of schizophrenia, emphasizing the necessity of ongoing research to refine and optimize its efficacy across diverse symptom domains.

Increased functional connectivity between brain regions involved in social cognition, emotion and affective-value in psychedelic states induced by N,N-Dimethyltryptamine (DMT)

The modulation of social cognition is suggested as a possible mechanism contributing to the potential clinical efficacy of psychedelics in disorders involving socio-emotional and reward processing deficits. Resting-state functional Magnetic Resonance Imaging (rs-fMRI) can be used to detect changes in brain connectivity during psychedelic-induced states. Thus, this pharmacoimaging study investigates the effects of N,N-Dimethyltryptamine (DMT) on functional connectivity in brain areas relevant to social cognition, using a within-subject design in eleven healthy experienced users. The study included both an active and a control condition, conducted at different time points. The active condition involved DMT inhalation, while the control condition did not. Seed-based connectivity was measured for the two core regions involved in theory of mind and emotional processing, respectively, the posterior supramarginal gyrus and the amygdala. DMT increased supramarginal gyrus connectivity with the precuneus, posterior cingulate gyrus, amygdala, and orbitofrontal cortex. Additionally, increased connectivity emerged between the amygdala and orbitofrontal cortex. These results demonstrate that DMT modulates brain connectivity in socio-emotional and affective-value circuits, advancing our understanding of the neural mechanisms underlying the psychedelic experience and its potential therapeutic action.