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CONTEXT: Pain-related movement fear is a contributing factor to residual pain and functional deficits in chronic ankle instability (CAI), but its underlying neural mechanisms remain unclear. OBJECTIVES: We aimed to (1) delineate whether participants with CAI exhibit discernible differences in specific emotion and pain-related brain regions, compared to a healthy control (HC) cohort and (2) explore potential neural mechanisms underlying pain and fear in participants with CAI, with an emphasis on investigating possible associations with pain-related neural plasticity. DESIGN: Cross-sectional study. SETTING: University research laboratory. PATIENTS OR OTHER PARTICIPANTS: 28 participants with CAI (17males and 11 females; age: 31.28±6.31 years) and 28 HCs (16 males and 12 females; age: 30.18±7.59 years). MAIN OUTCOME MEASURE(S): We analyzed T1 structural imaging data from participants and assessed their fear of movement and pain intensity using the Tampa Scale for Kinesiophobia (TSK) and the Visual Analog Scale (VAS) for pain, respectively. We compared the mean gray matter (GM) density of pain-related area between the two groups and their correlations with the TSK and VAS scores. RESULTS: In comparison with the HC group, participants with CAI showed a significant decrease in the mean GM density in the prefrontal cortex (Cohen's d = -0.808) and periaqueductal gray (Cohen's d = -0.934). In participants with CAI, the mean GM density of the prefrontal cortex (PFC) was negatively correlated with the TSK scores (r = -0.531). During intense exercise, the mean GM density of the periaqueductal gray (PAG) was negatively correlated with the VAS scores (r = -0.484). Additionally, TSK scores were positively correlated with VAS scores (r = 0.455). CONCLUSIONS: Our exploratory findings suggest that, in participants with CAI, the atrophy of the PFC and PAG may be associated with pain-related fear. Future clinical diagnosis and treatment for CAI should consider the impact of psychological barriers on functional recovery.

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Head trauma often impairs cognitive processes mediated within the prefrontal cortex (PFC), leading to impaired decision making and risk-taking behavior. Mild traumatic brain injury (mTBI) accounts for approximately 80 % of reported head injury cases. Most neurological symptoms of a single mTBI are transient; however, growing evidence suggests that repeated mTBI (rmTBI) results in more severe impairments that worsen with each subsequent injury. Although mTBI-induced disruption of risk/reward decision making has been characterized, the potential for rmTBI to exacerbate these effects and the neural mechanisms involved are unknown. Catecholamine neurotransmitters, dopamine (DA) and norepinephrine (NE), modulate PFC-mediated functions. Imbalances in catecholamine function have been associated with TBI and may underlie aberrant decision making. We used a closed head-controlled cortical impact (CH-CCI) model in rats to evaluate the effects of rmTBI on performance of a probabilistic discounting task of risk/reward decision making behavior and expression levels of catecholamine regulatory proteins within the PFC. RmTBI produced transient increases in risky choice preference in both male and female rats, with these effects persisting longer in females. Additionally, rmTBI increased expression of the catecholamine synthetic enzyme, tyrosine hydroxylase (TH), within the orbitofrontal (OFC) region of the PFC in females only. These results suggest females are more susceptible to rmTBI-induced disruption of risk/reward decision making behavior and dysregulation of catecholamine synthesis within the OFC. Together, using the CH-CCI model of rodent rmTBI to evaluate the effects of multiple insults on risk-taking behavior and PFC catecholamine regulation begins to differentiate how mTBI occurrences affect neuropathological outcomes across different sexes.

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Background: Transcranial magnetic stimulation-electroencephalography (TMS-EEG) is a powerful technique to study the neuropathology and biomarkers of major depressive disorder (MDD). This study investigated cortical activity and its relationship with clinical symptoms and cognitive dysfunction in MDD patients by indexing TMS-EEG biomarkers in the dorsolateral prefrontal cortex (DLPFC). Methods: 133 patients with MDD and 76 healthy individuals participated in this study. Single-pulse TMS was performed on the left DLPFC to obtain TMS-evoked potential (TEP) indices. TMS-EEG waveforms and components were determined by global mean field amplitude. We used the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to measure participants' cognitive function. Results: Patients with MDD had a lower excitatory P180 index compared to healthy controls, and P180 amplitude was negatively correlated with the severity of depressive and anxiety symptoms in patients with MDD. In the MDD group, P30 amplitude was negatively associated with RBANS Visuospatial/ Constructional index and total score. Conclusions: TMS-EEG findings suggest that abnormal cortical excitation and inhibition induced by TMS on the DLPFC are associated with the severity of clinical symptoms and cognitive dysfunction in patients with MDD. P180 and P30 have the potential to serve as neurophysiological biomarkers of clinical symptoms and cognitive dysfunction in MDD patients, respectively.

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Adolescence is an important phase for the structural and functional development of the brain. The immaturity of adolescent brain development is associated with high susceptibility to exogenous disturbances, including alcohol. In this study, the acquisition of conditioned place preference (CPP) in adolescent mice by alcohol (2 g/kg) and the parvalbumin-positive interneurons (PV+ interneurons), oligodendrocyte lineage cells (OPCs), and myelination in the medial prefrontal cortex (mPFC) were assessed. We aim to determine the age- and subregional-specificity of the effects of alcohol. Alcohol (2 g/kg) was injected intraperitoneally on even days, and saline was injected intraperitoneally on odd days. The control group received a continuous intraperitoneal injection with saline. Differences in alcohol-induced CPP acquisition were assessed, followed by immunohistochemical staining. The results showed a pronounced CPP acquisition in 4- and 5-week-old mice. In the mPFC, there were reduced PV+ interneurons and OPCs in 3-week-old mice and reduced oligodendrocyte numbers in 4-week-old mice. The 5-week-old mice showed impaired myelination and a decrease in the number of PV+ interneurons, mature oligodendrocytes, and OPCs in the mPFC. Since the alterations in 5-week-old mice are more pronounced, we further explored the mPFC-associated subregional-specificity. In the alcohol-exposed mice, the oligodendrocyte numbers were decreased in the anterior cingulate cortex (ACC), PV+ interneuron numbers were declined in the prelimbic cortex (PL), and the number of oligodendrocytes, PV+ interneurons, and OPCs was also decreased with impaired myelination in the infralimbic cortex (IL). Our data suggest that adolescent alcohol exposure notably affected the acquisition of CPP, myelin formation, and the counts of PV+ interneurons, mature oligodendrocytes, and OPCs in the mPFC in 5-week-old mice. Also, the IL subregion was the worst-affected subregion of the mPFC in alcohol-exposed 5-week-old mice. It reveals that the effects of alcohol on adolescence and its mPFC myelination show obvious age- and subregional-specificity.

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Background: Exciting left DLPFC activity with high frequency and inhibiting right DLPFC with low frequency repetitive transcranial magnetic stimulation (rTMS) has shown antidepressant effects in major depressive disorder (MDD) and executive functions. However, few studies have directly compared unilateral and bilateral protocols. Methods: Forty-seven individuals with treatment-resistant MDD underwent 10 sessions of rTMS over left DLPFC (20 Hz), bilateral DLPFC (left 20 Hz, right 1 Hz), or sham stimulation. Outcomes were depression (Beck Depression Inventory-II), visual-spatial memory (Corsi Block Test), response inhibition (Go/No-Go task), and cognitive flexibility (Wisconsin Card Sorting Test) assessed before and after treatment. Results: Both unilateral and bilateral rTMS significantly reduced depression levels versus sham controls based on BDI-II scores. While bilateral stimulation did not improve Corsi Test performance, unilateral protocol enhanced visual-spatial memory. On the Go/No-Go task, accuracy was higher in both active stimulation groups compared to sham, with no response time differences. Neither unilateral nor bilateral rTMS had significant effects on cognitive flexibility per the WCST. Conclusions: Despite comparable antidepressant effects, unilateral stimulation had some cognitive advantages over bilateral rTMS, potentially due to greater left dorsolateral prefrontal cortex excitation. Further research on parameter optimization is warranted.

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Major depressive disorder (MDD) is a psychiatric disorder characterized by depressed mood, behavioral despair and anhedonia. Demyelination in specific brain regions underlies the pathology of MDD, raising the alleviating demyelination as a potential strategy for MDD therapy. Nervonic acid (NA) has the potential to improve brain demyelination, offering benefits for various neurological disorders. However, its effects on depression remain undetermined. Mice were subjected to 14 days of chronic restraint stress (CRS) to induce depression-like behaviors, and were injected with NA (70 mg/kg) daily. The administration of NA significantly improved depressive-like behaviors in CRS mice. CRS led to significant demyelination in the medial prefrontal cortex (mPFC), which were reversed by NA treatment. In addition, NA ameliorated the upregulation of inflammatory cytokines and downregulation of brain-derived neurotrophic factor, improved the alternations in axonal spines observed in the mPFC of CRS mice. Our results highlighted the potential of NA as an antidepressant, with its benefits likely attributed to its effects in alleviating demyelination in the mPFC.

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Aberrant structural covariance (SC) in the medial prefrontal cortex (mPFC) is believed to play a crucial role in adolescent-onset major depressive disorder (AO-MDD). However, the effect of childhood abuse (CA) on SC in AO-MDD patients is still unknown. Here, we measured anomalous SC in the mPFC of AO-MDD patients and assessed the potential modulation of this feature by CA. We acquired T1-weighted structural images of AO-MDD patients (n = 93) and healthy controls (HCs, n = 81). Using voxel-based morphometry analysis, we calculated gray matter volumes for each subject. Subsequently, we classified abnormal SC in the mPFC into three subtypes according to overall CA. Compared with HCs, AO-MDD patients showed alterations in the structural covariance network of the mPFC, which is a central region in the default mode network (DMN). We also found an anterior-posterior dissociation in the structural covariance connectivity of the DMN. A history of CA modulated bilateral mPFC SC. These changes were primarily focused on the SC between the mPFC and the limbic system, indicating a gap in the rate of neural maturation between these regions. In summary, the DMN and frontal-limbic system, which are involved in emotional processing, appear to play a significant role in the development of AO-MDD. These findings highlight the crucial effects of CA on neurophysiological alterations in individuals with AO-MDD.

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In order to understand how prefrontal cortex provides the benefits of working memory (WM) for visual processing we examined the influence of WM on the representation of visual signals in V4 neurons in two macaque monkeys. We found that WM induces strong ß oscillations in V4 and that the timing of action potentials relative to this oscillation reflects sensory information- i.e., a phase coding of visual information. Pharmacologically inactivating the Frontal Eye Field part of prefrontal cortex, we confirmed the necessity of prefrontal signals for the WM-driven boost in phase coding of visual information. Indeed, changes in the average firing rate of V4 neurons could be accounted for by WM-induced oscillatory changes. We present a network model to describe how WM signals can recruit sensory areas primarily by inducing oscillations within these areas and discuss the implications of these findings for a sensory recruitment theory of WM through coherence.

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Early life stress alters gut microbiota and increases the risk of neuropsychiatric disorders, including social deficits and anxiety, in the host. However, the role of gut commensal bacteria in early life stress-induced neurobehavioral abnormalities remains unclear. Using the maternally separated (MS) mice, our research has unveiled a novel aspect of this complex relationship. We discovered that the reduced levels of amino acid transporters in the intestine of MS mice led to low glutamine (Gln) levels in the blood and synaptic dysfunction in the medial prefrontal cortex (mPFC). Abnormally low blood Gln levels limit the brain's availability of Gln, which is required for presynaptic glutamate (Glu) and γ-aminobutyric acid (GABA) replenishment. Furthermore, MS resulted in gut microbiota dysbiosis characterized by a reduction in the relative abundance of Lactobacillus reuteri (L. reuteri). Notably, supplementation with L. reuteri ameliorates neurobehavioral abnormalities in MS mice by increasing intestinal amino acid transport and restoring synaptic transmission in the mPFC. In conclusion, our findings on the role of L. reuteri in regulating intestinal amino acid transport and buffering early life stress-induced behavioral abnormalities provide a novel insight into the microbiota-gut-brain signaling basis for emotional behaviors.

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Alzheimer's disease (AD), the leading cause of dementia, is a multifactorial disease influenced by aging, genetics, and environmental factors. miRNAs are crucial regulators of gene expression and play significant roles in AD onset and progression. This exploratory study analyzed the expression levels of 28 genes and 5 miRNAs (miR-124-3p, miR-125b-5p, miR-21-5p, miR-146a-5p, and miR-155-5p) related to AD pathology and neuroimmune responses using RT-qPCR. Analyses were conducted in the prefrontal cortex (PFC) and the hippocampus (HPC) of the 5xFAD mouse AD model at 6 and 9 months old. Data highlighted upregulated genes encoding for glial fibrillary acidic protein (Gfap), triggering receptor expressed on myeloid cells (Trem2) and cystatin F (Cst7), in the 5xFAD mice at both regions and ages highlighting their roles as critical disease players and potential biomarkers. Overexpression of genes encoding for CCAAT enhancer-binding protein alpha (Cebpa) and myelin proteolipid protein (Plp) in the PFC, as well as for BCL2 apoptosis regulator (Bcl2) and purinergic receptor P2Y12 (P2yr12) in the HPC, together with upregulated microRNA(miR)-146a-5p in the PFC, prevailed in 9-month-old animals. miR-155 positively correlated with miR-146a and miR-21 in the PFC, and miR-125b positively correlated with miR-155, miR-21, while miR-146a in the HPC. Correlations between genes and miRNAs were dynamic, varying by genotype, region, and age, suggesting an intricate, disease-modulated interaction between miRNAs and target pathways. These findings contribute to our understanding of miRNAs as therapeutic targets for AD, given their multifaceted effects on neurons and glial cells.

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BACKGROUND: Emotional dysregulation is a serious and impairing mental health problem. We examined functional activity and connectivity of neural networks involved in emotional dysregulation at baseline and following a pilot neurostimulation-enhanced cognitive restructuring intervention in a transdiagnostic clinical adult sample. METHODS: Neuroimaging data were analyzed from adults who scored 89 or higher on the Difficulties with Emotion Regulation (DERS) scale and had at least one DSM-5 diagnosis. These participants were part of a pilot randomized, double-blind, placebo-controlled trial combining a single therapeutic session of cognitive restructuring with active or sham transcranial magnetic stimulation over the dorsolateral prefrontal cortex. During the study, participants engaged in an emotional regulation task using personalized autobiographical stressors while undergoing functional magnetic resonance imaging (fMRI) before and after the pilot intervention. The fMRI task required participants to either experience the emotions associated with the memories or apply cognitive restructuring strategies to reduce their distress. RESULTS: Whole-brain fMRI results during regulation at baseline revealed increased activation in the dorsal frontoparietal network but decreased activation in the supplementary motor area, cingulate cortex, insula, and ventrolateral prefrontal cortex (vlPFC). Emotion dysregulation was associated with greater vmPFC and amygdala activation and functional connectivity between these regions. The strength of functional connectivity between the dlPFC and other frontal regions was also a marker of emotional dysregulation. Preliminary findings from a subset of participants who completed the follow-up fMRI scan showed that active neurostimulation improved behavioral indices of emotion regulation more than sham stimulation. A whole-brain generalized psychophysiological interaction analysis indicated that active neurostimulation selectively increased occipital cortex connectivity with both the insula and the dlPFC. Region-of-interest functional connectivity analyses showed that active neurostimulation selectively increased dlPFC connectivity with the insula and orbitofrontal cortex (OFC). CONCLUSION: Insufficient neural specificity during the emotion regulation process and over-involvement of frontal regions may be a marker of emotional dysregulation across disorders. OFC, vlPFC, insula activity, and connectivity are associated with improved emotion regulation in transdiagnostic adults. In this pilot study, active neurostimulation led to neural changes in the emotion regulation network after a single session; however, the intervention findings are preliminary, given the small sample size. These functional network properties can inform future neuroscience-driven interventions and larger-scale studies.

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How consciousness is lost in states such as sleep or anesthesia remains a mystery. To gain insight into this phenomenon, concurrent recordings of electrophysiology signals in the anterior cingulate cortex and whole-brain functional magnetic resonance imaging (fMRI) are conducted in rats exposed to graded propofol, undergoing the transition from consciousness to unconsciousness. The results reveal that upon the loss of consciousness (LOC), there is a sharp increase in low-frequency power of the electrophysiological signal. Additionally, fMRI signals exhibit a cascade of deactivation across a pathway including the hippocampus, thalamus, and medial prefrontal cortex (mPFC) surrounding the moment of LOC, followed by a broader increase in brain activity across the cortex during sustained unconsciousness. Furthermore, sliding window analysis demonstrates a temporary increase in synchrony of fMRI signals across the hippocampus-thalamus-mPFC pathway preceding LOC. These data suggest that LOC may be triggered by sequential activities in the hippocampus, thalamus, and mPFC, while wide-spread activity increases in other cortical regions commonly observed during anesthesia-induced unconsciousness may be a consequence, rather than a cause of LOC. Taken together, the study identifies a cascade of neural events unfolding as the brain transitions into unconsciousness, offering insight into the systems-level neural mechanisms underpinning LOC.

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Introduction: Perturbation walking (PW) has been shown to improve gait, however its effect on the cortical control of gait might provide insights on neural mechanisms underlying falls in adults with osteoarthritis. The objective of this study is to investigate the effect of PW on prefrontal cortical (PFC) activation in older women with (OA) and without osteoarthritis (HOA). We hypothesized that there would be an increase in PFC activation during PW relative to comfortable walking (CW) and higher increase in PFC activation during PW in HOA compared to OA. Methods: Twenty community-dwelling older women (66.7 ± 5.41 years old) walked on an instrumented treadmill that provided perturbations at pseudo-random intervals between 5-25 s using a counterbalanced design. Functional Near Infrared Spectroscopy was used to quantify PFC oxygenated hemoglobin (HbO2) and deoxyhemoglobin (Hb) levels, while standing prior to the task as a baseline. A linear mixed effects model was conducted to investigate the effects of cohort (HOA vs OA), task (PW vs CW), and their interaction on HbO2 (µM) and Hb (µM) levels. Results: HbO2 and Hb levels differed significantly between CW and PW tasks for both cohorts (P < 0.001) and demonstrated significant task by cohort interaction (P < 0.05). In addition, we found changes in walking performance (stride time, stride length, stride width and stance time) during and after PW. Spearman correlation demonstrated a strong association between increased stance time, increased body mass index and decreased PFC activation during PW. No other significant results were found. Discussion: This study found increase in PFC activation during PW and gait adaptation after a short bout of PW in HOA and OA. This increase in PFC activation was higher in HOA compared to OA, particularly during PW tasks, and was consistent with theory of limitations in mobility affecting neural activation in older adults. Further work remains to examine how pain, obesity, and mobility impacts cortical control in older adults with and without osteoarthritis.

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Normal aging is accompanied by changes in brain structure and function associated with cognitive decline. Structural and functional abnormalities, particularly the prefrontal cortex (PFC) and subcortical regions, contributed to cognitive aging. However, it remains unclear how the synchronized changes in structure and function of individual brain regions affect the cognition in aging. Using 3D T1-weighted structural data and movie watching functional magnetic resonance imaging data in a sample of 422 healthy individuals (ages from 18 to 87 years), we constructed regional structure-function coupling (SFC) of cortical and subcortical regions by quantifying the distribution similarity of gray matter volume (GMV) and amplitude of low-frequency fluctuation (ALFF). Further, we investigated age-related changes in SFC and its relationship with cognition. With aging, increased SFC localized in PFC, thalamus and caudate nucleus, decreased SFC in temporal cortex, lateral occipital cortex and putamen. Moreover, the SFC in the PFC was associated with executive function and thalamus was associated with the fluid intelligence, and partially mediated age-related cognitive decline. Collectively, our results highlight that tighter structure-function synchron of the PFC and thalamus might contribute to age-related cognitive decline, and provide insight into the substrate of the thalamo-prefrontal pathway with cognitive aging.

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The question of how consciousness and behavior arise from neural activity is fundamental to understanding the brain, and to improving the diagnosis and treatment of neurological and psychiatric disorders. There is significant murine and primate literature on how behavior is related to the electrophysiological activity of the medial prefrontal cortex and its role in working memory processes such as planning and decision-making. Existing experimental designs, specifically the rodent spike train and local field potential recordings during the T-maze alternation task, have insufficient statistical power to unravel the complex processes of the prefrontal cortex. We therefore examined the theoretical limitations of such experiments, providing concrete guidelines for robust and reproducible science. To approach these theoretical limits, we applied dynamic time warping and associated statistical tests to data from neuron spike trains and local field potentials. The goal was to quantify neural network synchronicity and the correlation of neuroelectrophysiology with rat behavior. The results show the statistical limitations of existing data, and the fact that making meaningful comparison between dynamic time warping with traditional Fourier and wavelet analysis is impossible until larger and cleaner datasets are available.

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Background: Evidence from animal and human studies suggests glutamatergic dysfunction in posttraumatic stress disorder (PTSD). The purpose of this study was to investigate glutamate abnormalities in the dorsolateral prefrontal cortex (DLFPC) of individuals with PTSD using 7T MRS, which has better spectral resolution and signal-to-noise ratio than lower field strengths, thus allowing for better spectral quality and higher sensitivity. We hypothesized that individuals with PTSD would have lower glutamate levels compared to trauma-exposed individuals without PTSD and individuals without trauma exposure. Additionally, we explored potential alterations in other neurometabolites and the relationship between glutamate and psychiatric symptoms. Methods: Individuals with PTSD (n = 27), trauma-exposed individuals without PTSD (n = 27), and individuals without trauma exposure (n = 26) underwent 7T MRS to measure glutamate and other neurometabolites in the left DLPFC. The severities of PTSD, depression, anxiety, and dissociation symptoms were assessed. Results: We found that glutamate was lower in the PTSD and trauma-exposed groups compared to the group without trauma exposure. Furthermore, N-acetylaspartate (NAA) was lower and lactate was higher in the PTSD group compared to the group without trauma exposure. Glutamate was negatively correlated with depression symptom severity in the PTSD group. Glutamate was not correlated with PTSD symptom severity. Conclusion: In this first 7T MRS study of PTSD, we observed altered concentrations of glutamate, NAA, and lactate. Our findings provide evidence for multiple possible pathological processes in individuals with PTSD. High-field MRS offers insight into the neurometabolic alterations associated with PTSD and is a powerful tool to probe trauma- and stress-related neurotransmission and metabolism in vivo.

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Parkinson disease (PD) is a neurodegenerative disorder that causes motor and cognitive deficits, presenting complex challenges for therapeutic interventions. Repetitive transcranial magnetic stimulation (rTMS) is a type of neuromodulation that can produce plastic changes in neural activity. rTMS has been trialed as a therapy to treat motor and non-motor symptoms in persons with Parkinson disease (PwP), particularly treatment-refractory postural instability and gait difficulties such as Freezing of Gait (FoG), but clinical outcomes have been variable. We suggest improving rTMS neuromodulation therapy for balance and gait abnormalities in PwP by targeting brain regions in cognitive-motor control networks. rTMS studies in PwP often targeted motor targets such as the primary motor cortex (M1) or supplementary motor area (SMA), overlooking network interactions involved in posture-gait control disorders. We propose a shift in focus toward alternative stimulation targets in basal ganglia-cortex-cerebellum networks involved in posture-gait control, emphasizing the dorsolateral prefrontal cortex (dlPFC), cerebellum (CB), and posterior parietal cortex (PPC) as potential targets. rTMS might also be more effective if administered during behavioral tasks designed to activate posture-gait control networks during stimulation. Optimizing stimulation parameters such as dosage and frequency as used clinically for the treatment of depression may also be useful. A network-level perspective suggests new directions for exploring optimal rTMS targets and parameters to maximize neural plasticity to treat postural instabilities and gait difficulties in PwP.

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Background: Anodal transcranial direct current stimulation (tDCS) over the right dorsolateral prefrontal cortex (DLPFC) has shown to have effects on different domains of cognition yet there is a gap in the literature regarding effects on reflective thinking performance. Objective: The current study investigated if single session and repeated anodal tDCS over the right DLPFC induces effects on judgment and decision-making performance and whether these are linked to working memory (updating) performance or cognitive inhibition. Methods: Participants received anodal tDCS over the right DLPFC once (plus sham tDCS in a second session) or twice (24 h apart). In the third group participants received a single session of sham stimulation only. Cognitive characteristic measures were administered pre-stimulation (thinking disposition, impulsivity, cognitive ability). Experimental tasks included two versions of the Cognitive Reflection Test (numeric vs verbal-CRT), a set of incongruent base-rate vignettes, and two working memory tests (Sternberg task and n-back task). Forty-eight participants (mean age = 26.08 ± 0.54 years; 27 females) were recruited. Results: Single sessions of tDCS were associated with an increase in reflective thinking performance compared to the sham conditions, with stimulation improving scores on incongruent base rate tasks as well as marginally improving numeric CRT scores (compared to sham), but not thinking tasks without a numeric component (verbal-CRT). Repeated anodal stimulation only improved numeric CRT scores. tDCS did not increase working memory (updating) performance. These findings could not be explained by a practice effect or a priori differences in cognitive characteristics or impulsivity across the experimental groups. Conclusion: The current results demonstrate the involvement of the right DLPFC in reflective thinking performance which cannot be explained by working memory (updating) performance or general cognitive characteristics of participants.

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The regulation of emotions is a crucial facet of well-being and social adaptability, with explicit strategies receiving primary attention in prior research. Recent studies, however, emphasize the role of implicit emotion regulation, particularly implicating the ventromedial prefrontal cortex (VMPFC) in association with its implementation. This study delves into the nuanced role of the VMPFC through focality-optimized multichannel transcranial direct current stimulation (tDCS), shedding light on its causal involvement in implicit reappraisal. The primary goal was to evaluate the effectiveness of VMFPC-targeted tDCS and elucidate its role in individuals with high trait anxiety. Participants engaged in implicit and explicit emotion regulation tasks during multichannel tDCS targeting the VMPFC. The outcome measures encompassed negative emotion ratings, pupillary diameter, and saccade count, providing a comprehensive evaluation of emotion regulation efficiency. The intervention exhibited a notable impact, resulting in significant reductions in negative emotion ratings and pupillary reactions during implicit reappraisal, highlighting the indispensable role of the VMPFC in modulating emotional responses. Notably, these effects demonstrated sustained efficacy up to 1 day postintervention. This study underscores the potency of VMPFC-targeted multichannel tDCS in augmenting implicit emotion regulation. This not only contributes insights into the neural mechanisms of emotion regulation but also suggests innovative therapeutic avenues for anxiety disorders. The findings present a promising trajectory for future mood disorder interventions, bridging the gap between implicit emotion regulation and neural stimulation techniques.

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Major depressive disorder (MDD) is a psychiatric disorder with several effective therapeutic approaches, being antidepressants and psychotherapies the first-line treatments. Nonetheless, due to side effects, limited efficacy, and contraindications for these treatments, alternative treatment options are required. Neurostimulation is a non-pharmacological and non-psychotherapeutic approach that has been under study for diverse neuropsychiatric conditions in the form of electrical or magnetic stimulation of the brain. Repetitive transcranial magnetic stimulation (rTMS) is a neurostimulation method designed to generate magnetic fields and deliver magnetic pulses to stimulate the brain cortex. The magnetic pulses produce electrical currents in the brain which are not intense enough to provoke seizures, differentiating this method from other forms of neurostimulation that produce seizures. Although the exact rTMS mechanisms of action are not completely understood, rTMS seems to cause its beneficial effects through changes in neuroplasticity. Devices and protocols for rTMS are still evolving, becoming more efficient over time. There are still some challenges to be addressed, including further refinement of parameters (coil/device type, location, intensity, frequency, number of sessions, and duration of treatment); treatment cost and burden for patients; and treatment resistance. However, the efficacy, tolerability, and safety of some rTMS protocols have been demonstrated in different double-blind sham-controlled randomized controlled trials and meta-analyses for treatment-resistant depression.

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