Parietal Cortex Research Articles

Functional and connectivity correlates associated with Parkinson's disease psychosis: a systematic review.

Neural underpinnings of Parkinson's disease psychosis remain unclear to this day with relatively few studies and reviews available. Using a systematic review approach, here, we aimed to qualitatively synthesize evidence from studies investigating Parkinson's psychosis-specific alterations in brain structure, function or chemistry using different neuroimaging modalities. PubMed, Web of Science and Embase databases were searched for functional MRI (task-based and resting state), diffusion tensor imaging, PET and single-photon emission computed tomography studies comparing Parkinson's disease psychosis patients with Parkinson's patients without psychosis. We report findings from 29 studies (514 Parkinson's psychosis patients, mean age ± SD = 67.92 ± 4.37 years; 51.36% males; 853 Parkinson's patients, mean age ± SD = 66.75 ± 4.19 years; 55.81% males). Qualitative synthesis revealed widespread patterns of altered brain function across task-based and resting-state functional MRI studies in Parkinson's psychosis patients compared with Parkinson's patients without psychosis. Similarly, white matter abnormalities were reported in parietal, temporal and occipital regions. Hypo-metabolism and reduced dopamine transporter binding were also reported whole brain and in sub-cortical areas. This suggests extensive alterations affecting regions involved in high-order visual processing and attentional networks.

The participation of monoamines in the realization of vasopressin analgesic effects during electrical stimulation of paws in rats

BACKGROUND: Arginine vasopressin has been implicated in the modulation of stress and pain. The influence of a synthetic analogue of arginine vasopressin, 1-deamino-8-D-arginine-vasopressin, оn pain sensitivity, stress reactivity, levels of monoamines and brain neurotrophic factor in a model of paw electrical stimulation in rats has not been studied. AIM: The aim was to evaluate the effect of a synthetic vasopressin analog, 1-deamino-8-D-arginine-vasopressin, on pain sensitivity and the content of norepinephrine, serotonin, dopamine, brain neurotrophic factor in the parietal cortex and spinal cord in electrocutaneous paw stimulation test in rats. MATERIALS AND METHODS: The study was conducted on male Wistar rats who were injected with 1-deamino-8-D-arginine-vasopressin intranasally once a day for 5 days in small (single 20 ng, course 100 ng) and large doses (single 2 ug, course 10 ug). The content of brain neurotrophic factor in the parietal cortex and spinal cord, and corticosterone in blood serum were determined using enzyme immunoassay. The levels of norepinephrine, serotonin, dopamine and their metabolites in the brain were evaluated using high-performance liquid chromatography. RESULTS: 1-Deamino-8-D-arginine-vasopressin in different doses reduced pain sensitivity in rats, more pronounced when administered in large doses. The peptide in small doses in the parietal cortex increased the content of dopamine and reduced the levels of 5-hydroxyindolacetic acid, a metabolite of serotonin; in the spinal cord, it reduced the content of 5-hydroxyindolacetic acid. 1-Deamino-8-D-arginine-vasopressin in high doses in the parietal cortex increased the content of dopamine and reduced the levels of 5-hydroxyindolacetic acid; in the spinal cord ― reduced the content of serotonin and 3,4-dihydroxyphenylacetic acid, a metabolite of dopamine; increased the levels of norepinephrine and homovanilic acid, a metabolite of dopamine. The peptide had no effect on corticosterone levels in the blood and brain neurotrophic factor levels in the brain in rats. CONCLUSIONS: The analgesic effects of 1-deamino-8-D-arginine-vasopressin were revealed with intranasal administration in different subendocrine doses. Regardless of the administered doses, dopamine and serotonin at the supraspinal level were involved in peptide-induced anesthesia; serotonin at the spinal cord level. More pronounced analgesia with the administration of 1-deamino-8-D-arginine-vasopressin in high doses was due to the additional involvement of dopamine and norepinephrine at the spinal cord level.

Zero-shot counting with a dual-stream neural network model.

To understand a visual scene, observers need to both recognize objects and encode relational structure. For example, a scene comprising three apples requires the observer to encode concepts of "apple" and "three." In the primate brain, these functions rely on dual (ventral and dorsal) processing streams. Object recognition in primates has been successfully modeled with deep neural networks, but how scene structure (including numerosity) is encoded remains poorly understood. Here, we built a deep learning model, based on the dual-stream architecture of the primate brain, which is able to count items "zero-shot"-even if the objects themselves are unfamiliar. Our dual-stream network forms spatial response fields and lognormal number codes that resemble those observed in the macaque posterior parietal cortex. The dual-stream network also makes successful predictions about human counting behavior. Our results provide evidence for an enactive theory of the role of the posterior parietal cortex in visual scene understanding.

Effects of ketamine on frontoparietal interactions in a rule-based antisaccade task in macaque monkeys.

Cognitive control is engaged by working memory processes and high-demand situations like antisaccade, where one must suppress a prepotent response. While it is known to be supported by the frontoparietal control network, how intra- and inter-areal dynamics contribute to cognitive control processes remain unclear. N-Methyl-D-aspartate glutamate receptors (NMDARs) play a key role in prefrontal dynamics that support cognitive control, and its antagonists, such as ketamine, are known to alter task-related prefrontal activities and impair cognitive performance. However, the role of NMDAR in cognitive control-related frontoparietal dynamics remain underexplored. Here, we simultaneously recorded local field potentials and single unit activities from lateral prefrontal (lPFC) and posterior parietal cortices (PPC) in two male macaque monkeys during a rule-based antisaccade task, with both Rule-Visible (RV) and Rule-Memorized (RM) conditions. In addition to altering the E/I balance in both areas, ketamine had a negative impact on rule-coding in true oscillatory activities. It also reduced frontoparietal coherence in a frequency- and rule-dependent manner. Granger prediction analysis revealed that ketamine induced an overall reduction in bidirectional connectivity. Among antisaccade trials, a greater reduction in lPFC-PPC connectivity during the delay period preceded a greater delay in saccadic onset under the RM condition, and a greater deficit in performance under the RV condition. Lastly, ketamine compromised rule coding in lPFC neurons in both RV and RM conditions, and in PPC neurons only in the RV condition. Our findings demonstrate the utility of acute NMDA receptor antagonist in understanding the mechanisms through which frontoparietal dynamics support cognitive control processes.Significance statement A low dose of ketamine is known to induce a transient cognitive control deficit in healthy humans and animals, but it remains unclear whether this deficit is related to a frontoparietal dysconnection. In macaque monkeys performing a rule-based pro- and anti-saccade task, we found that ketamine impaired information coding in frontoparietal neuron, local oscillations and inter-areal synchrony in a rule- and frequency-dependent manner. Notably, under the antisaccade rule, the amount of impairment in task performance could be predicted by the loss in fronto-parietal connectivity in the period just before the monkeys responded. The observations support the utility of NMDA receptor antagonists like ketamine as a tool to understand the role of frontoparietal dynamics in cognitive control.

Acupuncture-assisted lifestyle intervention improve the metabolic status and spontaneous brain activity of type 2 diabetes Mellitus patients: a randomized, clinical trial

BackgroundAggressive weight management in patients with type 2 diabetes mellitus has demonstrated numerous metabolic advantages, however, existing therapies for weight control have not reached satisfactory results. This study aimed to evaluate the efficacy and safety of acupuncture in the weight management of type 2 diabetes mellitus (T2DM) patients by using a randomized, sham-controlled clinical trial design.MethodsIn this single-blind randomized clinical trial, 102 overweight adult T2DM patients were randomized into two groups. The control group receives diet, exercise, and sham acupuncture intervention, whereas the acupuncture group receives diet and exercise and acupuncture intervention, both for 1 month. Body weight and other anthropometric and laboratory indices were assessed at baseline and endpoint, meanwhile, the body fat content and spontaneous brain activity were measured by functional magnetic resonance imaging(fMRI)as the exploratory outcomes.ResultsNo significant difference was observed between the studied parameters at the baseline. The body weight and BMI were significantly reduced both in the control and acupuncture groups after intervention, without statistical difference between the two groups. What’s interesting is that compared to the control, the acupuncture group displayed a greater improvement in central fat tissue. It notes that the acupuncture group achieved significant liver fat content reduction than the sham acupuncture group. At the same time, the spontaneous brain activity in the occipital lobe and parietal lobe significantly increased in the acupuncture group.ConclusionOne month of acupuncture treatment preferentially improved ectopic fat deposition and was accompanied by changes in brain activity compared with the control group, even before significant changes in total body weight had occurred. further studies of longer duration are necessary for validation.Trial registration: The protocol of this clinical trial is registered at the Acupuncture-Moxibustion Clinical Trial Registry (AMCTR, http://www.acmctr.org/, No. AMCTR-IOR-20000341).

A quantitative analysis of bestrophin 1 cellular localization in mouse cerebral cortex.

Calcium-activated ligand-gated chloride channels, beyond their role in maintaining anion homeostasis, modulate neuronal excitability by facilitating nonvesicular neurotransmitter release. BEST1, a key member of this family, is permeable to γ-aminobutyric acid (GABA) and glutamate. While astrocytic BEST1 is well-studied and known to regulate neurotransmitter levels, its distribution and role in other brain cell types remain unclear. This study aimed to reassess the localization of BEST1 in the mouse cerebral cortex. We examined the localization and distribution of BEST1 in the mouse parietal cortex using light microscopy, confocal double-labeling with markers for astrocytes, neurons, microglia, and oligodendrocyte precursor cells, and 3D reconstruction techniques. In the cerebral cortex, BEST1 is more broadly distributed than previously thought. Neurons are the second most abundant BEST1+ cell type in the cerebral cortex, following astrocytes. BEST1 is diffusely expressed in neuronal somatic and neuropilar domains and is present at glutamatergic and GABAergic terminals, with a prevalence at GABAergic terminals. We also confirmed that BEST1 is expressed in cortical microglia and identified it in oligodendrocyte precursor cells, albeit to a lesser extent. Together, these findings suggest that BEST1's role in controlling neurotransmission may extend beyond astrocytes to include other brain cells. Understanding BEST1's function in these cells could offer new insights into the molecular mechanisms shaping cortical circuitry. Further research is needed to clarify the diverse roles of BEST1 in both normal and pathophysiological conditions.

Enhancing visual working memory in schizophrenia: effects of frontoparietal theta tACS in low-performing patients

Schizophrenia is a complex neuro-psychiatric disorder including positive symptoms, negative symptoms, and cognitive deficits. A key cognitive dysfunction in schizophrenia is a deficit in visual working memory (VWM). VWM involves three distinct stages: encoding, maintenance, and retrieval. The deficit in any one stage would produce the same symptom (i.e., poor VWM), although their causes are not the same. In this study, we used a retro-cue VWM task that provides helpful cues at different stages: early in maintenance (early cue), late in maintenance (late cue), or during retrieval (retrieval cue). This modification would help “tag” or identify the cognitive stage(s) most responsible for impaired VWM performance in schizophrenia. Additionally, we took advantage of this tagging feature and applied 6 Hz transcranial alternating current stimulation (tACS) over the right dorsolateral prefrontal cortex (DLPFC) and right posterior parietal cortex (PPC)—which has previously been shown to enhance VWM in low-performing healthy individuals—to examine whether tACS would improve a specific stage or all stages of VWM processing in schizophrenia. We observed that cues significantly enhanced performance in low-performing patients, who benefited equally from early and late maintenance cues, but not from retrieval cues. These low-performers also responded well to theta tACS in their overall VWM performance as opposed to a specific VWM stage. No improvement effect was observed in high-performing patients for both retro cue and tACS. Together, our data suggest that 1) low-performing patients’ VWM deficits likely stem from poor memory consolidation rather than retrieval, 2) right frontoparietal theta tACS can improve low-performing patients’ VWM performance, and 3) such facilitatory tACS effect is not selective of a specific VWM stage and thus is likely driven by an improvement in overall visual attention.

Cell-Specific Gene Expressions Underlie Selective White Matter Loss Vulnerability in Mild Traumatic Brain Injury.

Traumatic brain injury (TBI), a risk factor for later-life dementia, leads to salient brain atrophy, particularly in the white matter. It is not clear how white matter atrophy progresses or why some brain regions are damaged while others are spared. We hypothesized that spatial variations of cell-specific gene expression contributed to the selective white matter loss vulnerability following mild TBI (mTBI). Gene expression data were sourced from the publicly available Allen Human Brain Atlas, which comprises microarray data spanning nearly the entire brain, derived from six neurologically normal adult donors. A total of 100 patients with acute stage (within 7 days post-injury) mTBI were enrolled. Of these, 60 patients were followed up at 3 months post-injury and 37 were followed up at 6-12 months post-injury. In addition, 59 healthy controls (HCs), matched for age, gender, and education, were included for comparative analysis. White matter volume changes were analyzed at both the acute stage, 3 months, and 6-12 months follow-up in mTBI patients compared with HCs. Patients with mTBI exhibited significant white matter atrophy in the frontal, parietal, and temporal cortices at 3 months post-injury, which even persisted at 6-12 months follow-up. In addition, mTBI patients with cognitive deficits showed more severe brain atrophy compared with those without cognitive deficits. Crucially, the gene expression marking endothelial cells and S1 pyramidal neurons were associated with increased brain atrophy, whereas the gene expression marking microglia and CA1 pyramidal neurons were associated with decreased brain atrophy in mTBI patients at 3 months post-injury. Microglia and endothelial cells can explain 23.6% of regional variations in the white matter atrophy. These findings suggested that modulating cellular activation, especially by promoting microglial activation at 3 months post-injury, might be a promising approach to prevent white matter atrophy, enhance cognitive outcomes, and reduce the risk of later-life dementia.

Cross-modal representation of chewing food in posterior parietal and visual cortex.

Even though the oral cavity is not visible, food chewing can be performed without damaging the tongue, oral mucosa, or other intraoral parts, with cross-modal perception of chewing possibly critical for appropriate recognition of its performance. This study was conducted to clarify the relationship of chewing food cross-modal perception with cortex activities based on examinations of the posterior parietal cortex (PPC) and visual cortex during chewing in comparison with sham chewing without food, imaginary chewing, and rest using functional near-infrared spectroscopy. Additionally, the effects of a deafferent tongue dorsum on PPC/visual cortex activities during chewing performance were examined. The results showed that chewing food increased activity in the PPC/visual cortex as compared with imaginary chewing, sham chewing without food, and rest. Nevertheless, those activities were not significantly different during imaginary chewing or sham chewing without food as compared with rest. Moreover, subjects with a deafferent tongue dorsum showed reduced PPC/visual cortex activities during chewing food performance. These findings suggest that chewing of food involves cross-modal recognition, while an oral somatosensory deficit may modulate such cross-modal activities.

Delineating three distinct spatiotemporal patterns of brain atrophy in Parkinson's disease.

The clinical manifestation of Parkinson's disease exhibits significant heterogeneity in the prevalence of non-motor symptoms and the rate of progression of motor symptoms, suggesting that Parkinson's disease can be classified into distinct subtypes. In this study, we aimed to explore this heterogeneity by identifying a set of subtypes with distinct patterns of spatiotemporal trajectories of neurodegeneration. We applied Subtype and Stage Inference (SuStaIn), an unsupervised machine learning algorithm that combined disease progression modelling with clustering methods, to cortical and subcortical neurodegeneration visible on 3 T structural MRI of a large cross-sectional sample of 504 patients and 279 healthy controls. Serial longitudinal data were available for a subset of 178 patients at the 2-year follow-up and for 140 patients at the 4-year follow-up. In a subset of 210 patients, concomitant Alzheimer's disease pathology was assessed by evaluating amyloid-β concentrations in the CSF or via the amyloid-specific radiotracer 18F-flutemetamol with PET. The SuStaIn analysis revealed three distinct subtypes, each characterized by unique patterns of spatiotemporal evolution of brain atrophy: neocortical, limbic and brainstem. In the neocortical subtype, a reduction in brain volume occurred in the frontal and parietal cortices in the earliest disease stage and progressed across the entire neocortex during the early stage, although with relative sparing of the striatum, pallidum, accumbens area and brainstem. The limbic subtype represented comparative regional vulnerability, which was characterized by early volume loss in the amygdala, accumbens area, striatum and temporal cortex, subsequently spreading to the parietal and frontal cortices across disease stage. The brainstem subtype showed gradual rostral progression from the brainstem extending to the amygdala and hippocampus, followed by the temporal and other cortices. Longitudinal MRI data confirmed that 77.8% of participants at the 2-year follow-up and 84.0% at the 4-year follow-up were assigned to subtypes consistent with estimates from the cross-sectional data. This three-subtype model aligned with empirically proposed subtypes based on age at onset, because the neocortical subtype demonstrated characteristics similar to those found in the old-onset phenotype, including older onset and cognitive decline symptoms (P < 0.05). Moreover, the subtypes correspond to the three categories of the neuropathological consensus criteria for symptomatic patients with Lewy pathology, proposing neocortex-, limbic- and brainstem-predominant patterns as different subgroups of α-synuclein distributions. Among the subtypes, the prevalence of biomarker evidence of amyloid-β pathology was comparable. Upon validation, the subtype model might be applied to individual cases, potentially serving as a biomarker to track disease progression and predict temporal evolution.

White matter protection with insulin-like growth factor-1 after hypoxia-ischaemia in preterm foetal sheep.

Perinatal hypoxia-ischaemia in extremely preterm infants is associated with long-term neurodevelopmental impairment, for which there is no specific treatment. Insulin-like growth factor-1 can reduce acute brain injury, but its effects on chronic white matter injury after hypoxia-ischaemia are unclear. Preterm-equivalent foetal sheep (0.6 gestation) received either sham-asphyxia or asphyxia induced by umbilical cord occlusion for 30 min, and recovered for either 3 or 35 days after asphyxia. The 35 day recovery groups received either an intracerebroventricular infusion of insulin-like growth factor-1 (1 µg/24 h) or vehicle, from 3 to 14 days after asphyxia. Asphyxia was associated with ventricular enlargement, and loss of frontal and parietal white matter area (P < 0.05 versus sham-asphyxia). This was associated with reduced area fraction of myelin basic protein and numbers of oligodendrocyte transcription factor 2 and mature, anti-adenomatous polyposis coli-positive oligodendrocytes in periventricular white matter (P < 0.05), with persistent inflammation and caspase-3 activation (P < 0.05). Four of eight foetuses developed cystic lesions in temporal white matter. Prolonged infusion with insulin-like growth factor-1 restored frontal white matter area, improved numbers of oligodendrocyte transcription factor 2-positive and mature, anti-adenomatous polyposis coli-positive oligodendrocytes, with reduced astrogliosis and microgliosis after 35 days recovery (P < 0.05 versus asphyxia). One of four foetuses developed temporal cystic lesions. Functionally, insulin-like growth factor-1-treated foetuses had faster recovery of EEG power, but not spectral edge. Encouragingly, these findings show that delayed, prolonged, insulin-like growth factor-1 treatment can improve functional maturation of periventricular white matter after severe asphyxia in the very immature brain, at least in part by suppressing chronic neural inflammation.

Multinodular Vacuolating Neuronal Tumors: Symptomatic Presentation Versus Incidental Finding: Case Series and Literature Review

Background: Multinodular Vacuolating Neuronal Tumors (MVNTs) are mixed glial–neuronal brain lesions classified as World Health Organization (WHO) CNS grade 1 tumors, often associated with long-term epilepsy. First described by Huse et al. in 2013 and included in the WHO CNS classification in 2016, MVNTs present a range of clinical manifestations, from symptomatic to asymptomatic. They typically affect young to middle-aged adults and exhibit diverse presentations. Radiologically, MVNTs are usually supratentorial, frequently located in the temporal lobe but also observed in the frontal and parietal lobes. MRI is essential for diagnosis, revealing multiple coalescing subcortical or cortical nodules with hyperintense signals on T2-weighted/FLAIR sequences, often without peripheral edema or mass effects. Case Reports: This paper presents two cases: one symptomatic MVNT with significant clinical manifestations, and the other documenting an incidental finding of MVNT in an asymptomatic patient. One case shows typical temporal lobe localization, while the other highlights a rare frontal lobe localization, with clear radiological findings on T2/FLAIR sequences. Conclusions: These cases illustrate the varied clinical presentations of MVNTs and emphasize MRI’s critical role in diagnosis and management. Asymptomatic cases often require conservative management, stressing the avoidance of unnecessary invasive procedures and the importance of regular monitoring.

Neural Correlates of Psychedelic, Sleep, and Sedated States Support Global Theories of Consciousness.

Understanding neural mechanisms of consciousness remains a challenging question in neuroscience. A central debate in the field concerns whether consciousness arises from global interactions that involve multiple brain regions or focal neural activity, such as in sensory cortex. Additionally, global theories diverge between the Global Neuronal Workspace (GNW) hypothesis, which emphasizes frontal and parietal areas, and the Integrated Information Theory (IIT), which focuses on information integration within posterior cortical regions. To disentangle the global vs. local and frontoparietal vs. posterior dilemmas, we measured global functional connectivity and local neural synchrony with functional magnetic resonance imaging (fMRI) data across a spectrum of conscious states in humans induced by psychedelics, sleep, and deep sedation. We found that psychedelic states are associated with increased global functional connectivity and decreased local neural synchrony. In contrast, non-REM sleep and deep sedation displayed the opposite pattern, suggesting that consciousness arises from global brain network interactions rather than localized activity. This mirror-image pattern between enhanced and diminished states was observed in both anterior-posterior (A-P) and posterior-posterior (P-P) brain regions but not within the anterior part of the brain alone. Moreover, anterior transmodal regions played a key role in A-P connectivity, while both posterior transmodal and posterior unimodal regions were critical for P-P connectivity. Overall, these findings provide empirical evidence supporting global theories of consciousness in relation to varying states of consciousness. They also bridge the gap between two prominent theories, GNW and IIT, by demonstrating how different theories can converge on shared neuronal mechanisms.

Preventive treatment effects on brain structures and functions in patients with chronic migraine: A multimodel magnetic resonance imaging study.

Patients with chronic migraine (CM) often exhibit structural and functional alterations in pain-matrix regions, but it remains unclear how preventive treatment affects these changes. Therefore, this study aimed to investigate the structural and functional changes in pain-matrix regions in CM patients after 6-month treatment. A total of 24 patients with CM and 15 healthy controls were recruited for this study. Patients were divided into responder group (N = 9) and non-responder group (N = 15). After completing the Migraine Disability Assessment (MIDAS) questionnaire, all patients underwent whole-brain high-resolution T1-weighted images, diffusion-weighted imaging, and resting-state functional magnetic resonance imaging at baseline and 6-month follow-up. Whole brain gray matter volume and white matter diffusion indices were analyzed using voxel-based analysis. Structural and functional connectivity analyses were performed to understand brain changes in patients after 6-month preventive treatment. The responder group exhibited significantly higher MIDAS scores than the non-responder group at baseline, but no significant difference between the two groups at follow-up. No significant interval change was noted in gray matter volume, white matter diffusion indices, and structural connectivity in CM patients after 6-month treatment. Nonetheless, the functional connectivity was significantly increased between occipital, temporal lobes and cerebellum, and was significantly decreased between parietal and temporal lobes after 6-month preventive treatment. We concluded that resting-state functional connectivity was suitable for investigating the preventive treatment effect on CM patients.

Daily high-frequency transcranial random noise stimulation (hf-tRNS) for sleep disturbances and cognitive dysfunction in patients with mild vascular cognitive impairments: A study protocol for a pilot randomized controlled trial.

Poor sleep quality is increasingly considered to be an underlying cause of cerebrovascular diseases. This is a slowly progressing condition that gradually leads to vascular cognitive impairment and stroke during ageing. At present, randomized clinical trials examining the non-pharmacological therapies in the management of this comorbidity are very limited. Transcranial current stimulation (tCS) is a non-invasive technology for promoting cognitive function and treating brain disorders. As advanced modalities of tCS, transcranial random noise stimulation (tRNS) and transcranial alternating current stimulation (tACS), could deliver frequency-specific waveforms of currents that can modulate brain activities in a more specific manner. Chinese individuals between the ages of 60 and 90 years, who are right-handed and have mild vascular cognitive impairment (VCI) with sleep disturbances, will participate in a randomized study. They will undergo a 2-week intervention period where they will be randomly assigned to one of three groups: high-frequency (hf)-tRNS, 40 Hz tACS, or sham tCS. Each group will consist of 15 participants. Before the intervention, high-resolution magnetic resonance imaging (MRI) data will be used to create a computational head model for each participant. This will help identify the treatment target of left inferior parietal lobe (IPL). Throughout the study, comprehensive assessments will be conducted at multiple time points, including baseline, 2nd week, 6th week, and 12th week. These assessments will evaluate various factors such as sleep quality, domain-specific cognitive performance, and actigraphic records. In addition, the participants' adherence to the program and any potential adverse effects will be closely monitored throughout the duration of the intervention. The primary objective of this study is to examine the safety, feasibility, and effectiveness of hf-tRNS and 40 Hz tACS interventions targeting left IPL in individuals with mild vascular cognitive impairment (VCI) who experience sleep disturbances and cognitive dysfunction. Additionally, the study seeks to evaluate the program's adherence, tolerability, and any potential adverse effects associated with frequency-specific transcranial current stimulation (tCS). The findings from this research will contribute to a deeper understanding of the intricate relationship between oscillation, sleep, and cognition. Furthermore, the results will provide valuable insights to guide future investigations in the field of sleep medicine and neurodegenerative diseases. ClinicalTrials.gov Identifier: NCT06169254.

Inhibition of the inferior parietal lobe triggers state-dependent network adaptations

The human brain comprises large-scale networks that flexibly interact to support diverse cognitive functions and adapt to variability in daily life. The inferior parietal lobe (IPL) is a hub of multiple brain networks that sustain various cognitive domains. It remains unclear how networks respond to acute regional perturbations to maintain normal function. To provoke network-level adaptive responses to local inhibition, we combined offline transcranial magnetic stimulation (TMS) over left or right IPL with neuroimaging during attention, semantic and social cognition tasks, and rest. Across tasks, TMS specifically affected task-active network activity with inhibition and facilitation. Network interaction responses differed between rest and tasks. After TMS over both IPL regions, large-scale network interactions were exclusively facilitated at rest, but mainly inhibited during tasks. Overall, responses to TMS primarily occurred in and between domain-general default mode and frontoparietal subnetworks. These findings elucidate short-term adaptive plasticity in response to network node inhibition.

Long-term cognitive training enhances fluid cognition and brain connectivity in individuals with MCI

Amnestic mild cognitive impairment (aMCI) is a risk factor for Alzheimer’s disease (AD). Multi-domain cognitive training (CT) may slow cognitive decline and delay AD onset. However, most work involves short interventions, targeting single cognitive domains or lacking active controls. We conducted a single-blind randomized controlled trial to investigate the effect of a 6-month, multi-domain CT on Fluid Cognition, functional connectivity in memory and executive functioning networks (primary outcomes), and white matter microstructural properties (secondary outcome) in aMCI. Sixty participants were randomly assigned to either a multi-domain CT or crossword training (CW) group, and thirty-four participants completed the intervention. We found a significant group-by-time interaction in Fluid Cognition (p = 0.007, F (1,28) = 8.26, Cohen’s d = 0.38, 95% confidence interval [CI]: 2.45–14.4), with 90% of CT patients showing post-intervention improvements (p < 0.01, Cohen’sd = 0.7). The CT group also showed better post-intervention Fluid Cognition than healthy controls (HCs, N = 45, p = 0.045). Functional connectivity analyses showed a significant group-by-time interaction (Cohen’s d ≥ 0.8) in the dorsolateral prefrontal cortex (DLPFC) and inferior parietal cortex (IPC) networks. Specifically, CT displayed post-intervention increases whereas CW displayed decreases in functional connectivity. Moreover, increased connectivity strength between the left DLPFC and medial PFC was associated with improved Fluid Cognition. At a microstructural level, we observed a decline in fiber density (FD) for both groups, but the CT group declined less steeply (1.3 vs. 2%). The slower decline in FD for the CT group in several tracts, including the cingulum-hippocampus tract, was associated with better working memory. Finally, we identified regions in cognitive control and memory networks for which baseline functional connectivity and microstructural properties were associated with changes in Fluid Cognition. Long-term, multi-domain CT improves cognitive functioning and functional connectivity and delays structural brain decline in aMCI (ClinicalTrials.gov number: NCT03883308).

Study on the event-related potential in recognition of emotional words between typical “five-state personality”

Objective: To explore the event-related potential (ERP) differences of people with typical traditional Chinese medicine (TCM) “five-state personality” in the task of judging the emotional attributes (positive, neutral, and negative) of Chinese words. Methods: The “five-state personality test” was applied to screen the typical TCM “five-state personality”, and three groups were established including positive personality, negative personality, and atypical personality. The differences of electroencephalogram (EEG) components in the task of judging the emotional attributes of Chinese words were collected using ERPs. The 3 personality groups ×3 words with emotional attributes were analyzed by two-way analysis of variance (ANOVA). Results: The N1 and P300 components were induced successfully. The analysis on the mean values of corresponding electrodes in left frontal lobe, right frontal lobe, frontal lobe and parietal lobe showed that in the typical negative personality group, the absolute value of N1 amplitude was smaller in the prefrontal and frontal lobes, and the latency was shorter in the left frontal lobe, while in the typical positive personality group, the absolute value of N1 amplitude was larger in the left frontal lobe. In the prefrontal and frontal lobes, the N1 peak absolute value of negative words was higher and the latency was longer, and the N1 latency of neutral words was shorter. The N1 latency of positive words was shorter in the parietal lobe. In the right frontal and frontal lobes, the P300 peak of negative words was higher and the latency was longer, while the latency of positive words was longer in the parietal lobe. In addition, there was some interaction between personality groups and emotional attributes of words. Conclusion: When people with typical “five-state personality” judge the emotional attributes of words, the absolute value of N1 amplitude in left prefrontal lobe of typical positive personality group is high, while that of typical negative personality group was small and the latency is short. The P300 latency of negative words is longer in the right frontal and frontal lobes, and that of positive words is longer in the parietal lobes, with more significant difference in the positive personality group.

Multi-scale hierarchical brain regions detect individual and interspecies variations of structural connectivity in macaque monkeys and humans

Macaques are representative animal models in translational research. However, the distinct shape and location of the brain regions between macaques and humans prevents us from comparing the brain structure directly. Here, we calculated structural connectivity (SC) with multi-scale hierarchical regions of interest (ROIs) to parcel out human and macaque brain into 8 (level 1 ROIs), 28 (level 2 ROIs), or 46 (level 3 ROIs) regions, which consist of anatomically and functionally defined level 4 ROIs (around 100 parcellation of the brain). The SC with the level 1 ROIs showed lower individual and interspecies variation in macaques and humans. SC with level 2 and 3 ROIs shows that the several regions in frontal, temporal and parietal lobe show distinct connectivity between macaques and humans. Lateral frontal cortex, motor cortex and auditory cortex were shown to be important areas for interspecies differences. These results provide insights to use macaques as animal models for translational study.

Characteristics of Functional Connections and Topographical Properties Distinguished the Healthy State and Obsessive-Compulsive Disorder

Background: Obsessive-compulsive disorder (OCD) is characterized by alterations in brain connectivity, particularly within the default mode network (DMN) and the salience network (SN). Investigating these connectivity differences can provide a deeper understanding of the neural mechanisms underlying OCD. Methods: This cross-sectional study involved 58 patients diagnosed with OCD and 38 healthy control subjects, totaling 96 participants. Resting-state functional MRI (fMRI) data were acquired and analyzed using the CONN toolbox to examine functional connectivity within intrinsic resting-state networks. Graph theory metrics were applied to evaluate node connections and the overall network topology. Clinical symptoms were assessed using the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), and their correlations with connectivity patterns and graph-theory parameters were analyzed. Results: The OCD patients and healthy controls were matched in terms of age, gender, marital status, socioeconomic status, and handedness. However, OCD patients had significantly worse general health, quality of life, and higher levels of depression and anxiety. Network analyses revealed altered whole-brain connectivity in OCD patients, particularly within the DMN and the frontoparietal network. The most significant between-group connectivity differences were observed between the posterior parietal cortex (PPC) and the precuneus. Disruptions in the DMN, specifically altered connectivity between the medial prefrontal cortex and posterior cingulate cortex, and changes in the SN involving the anterior insula and anterior cingulate cortex, were significantly correlated with the severity of OCD symptoms. Conclusions: The findings suggest that OCD is associated with distinct alterations in DMN connectivity, which may play a critical role in the disorder's pathophysiology. These disruptions offer potential targets for therapeutic intervention. Further research is needed to explore these connectivity changes in larger cohorts and at various stages of OCD to better understand their clinical significance.