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•We propose a novel seed-based fiber streamline (sFS) analysis method.•Our method produces fiber clusters with consistent geometric structures.•Our method enables tract analysis along fiber clusters of a seed-based fiber network.•Our method could predict pain empathy in participants with chronic pain. Pain empathy, defined as the ability of one person to understand another person's pain, shows large individual variations. The anterior insula is the core region of the pain empathy network. However, the relationship between white matter (WM) properties of the fiber tracts connecting the anterior insula with other cortical regions and an individual's ability to modulate pain empathy remains largely unclear. In this study, we outline an automatic seed-based fiber streamline (sFS) analysis method and multivariate pattern analysis (MVPA) to predict the levels of pain empathy in healthy women and women with primary dysmenorrhoea (PDM). Using the sFS method, the anterior insula-based fiber tract network was divided into five fiber cluster groups. In healthy women, interindividual differences in pain empathy were predicted only by the WM properties of the five fiber cluster groups, suggesting that interindividual differences in pain empathy may rely on the connectivity of the anterior insula-based fiber tract network. In women with PDM, pain empathy could be predicted by a single cluster group. The mean WM properties along the anterior insular–rostroventral area of the inferior parietal lobule further mediated the effect of pain on empathy in patients with PDM. Our results suggest that chronic periodic pain may lead to maladaptive plastic changes, which could further impair empathy by making women with PDM feel more pain when they see other people experiencing pain. Our study also addresses an important gap in the analysis of the microstructural characteristics of seed-based fiber tract network.

Growing evidence suggests that corticospinal tract (CST) damage and microstructural integrity are key predictors of post-stroke motor impairment. However, their combined clinical utility-particularly in CST sub-pathways originating from non-primary motor cortical areas-remains underexplored. This study aimed to determine whether microstructural integrity and lesion load (LL) of each CST sub-pathway at 2 weeks predict motor outcomes at 2, 6, and 12 weeks post-stroke. Fifty seven participants completed motor and neuroimaging evaluations at 2 weeks post-stroke and underwent follow-up motor assessments at 6 ( = 37) and 12 weeks ( = 34). The integrity of the CSTs was quantified using diffusion spectrum imaging (DSI), while CST-LL was measured using structural magnetic resonance imaging, both based on the sensorimotor area tract template atlas. Stepwise multiple linear regression models were used to assess the predictive value of CST microstructural integrity and CST-LL in each sub-pathway at 2 weeks for motor function at 2, 6, and 12 weeks post-stroke. The results indicated CST integrity and CST-LL were both the main determinants of motor deficit at 2 weeks post-stroke. Specifically, the integrity of CSTs from the primary motor cortex (M1), reflected by fractional anisotropy, emerged as a significant predictor of post-stroke motor deficit at 2 weeks, whereas CST integrity from the dorsal premotor cortex (PMd), reflected by generalized fractional anisotropy, quantitative anisotropy, and radial diffusivity. CST-LL originating from non-M1 motor areas, such as primary sensory cortex (S1), were also the main determinants for motor impairment at 2 weeks post-stroke. However, compared to CST integrity, CST-LL from non-M1 motor areas, including both the PMd and S1, were more dominant predictors, explaining 68.3% ( = 0.683, < 0.001) and 79.5% ( = 0.795, < 0.001) of the variance in motor outcomes at 6 and 12 weeks. The microstructural integrity of the PMd tracts and CST-LL from the non-M1 motor areas may be promising biomarker for post-stroke motor impairment. These findings highlight the pivotal role of non-M1 tracts in post-stroke motor function, particularly the PMd tracts, as a potential intervention target to enhance motor recovery.

•At baseline, the gray matter volume (GMV) in the frontal-limbic network (i.e., the dorsolateral prefrontal cortex (DLPFC) and dorsal anterior cingulate cortex (dACC)) were associated with fatigue severity in individuals after a mild SARS-CoV-2 infection.•Acute fatigue mediated the associations between the volume differences in fatigue susceptibility and comorbid neuropsychiatric symptoms at baseline and 3 months after infection.•The GMV in the DLPFC at baseline can predict fatigue symptoms 3 months after infection.•Identifying early neurobiological markers to predict individuals at risk for developing persistent fatigue. Fatigue is often accompanied by comorbid sleep disturbance and psychiatric distress following the COVID-19 infection. However, identifying individuals at risk for developing post-COVID fatigue remains challenging. This study aimed to identify the neurobiological markers underlying fatigue susceptibility and further investigate their effect on COVID-19-related neuropsychiatric symptoms. Individuals following a mild SARS-CoV-2 infection (COV+) underwent neuropsychiatric measurements (n = 335) and MRI scans (n = 271) within 1 month (baseline), and 191 (70.5 %) of the individuals were followed up 3 months after infection. Sixty-seven healthy controls (COV−) completed the same recruitment protocol. Whole-brain voxel-wise analysis showed that gray matter volume (GMV) during the acute phase did not differ between the COV+ and COV− groups. GMV in the right dorsolateral prefrontal cortex (DLPFC) and left dorsal anterior cingulate cortex (dACC) were associated with fatigue severity only in the COV+ group at baseline, which were assigned to the frontal system and limbic system, respectively. Furthermore, fatigue mediated the associations between volume differences in fatigue susceptibility and COVID-related sleep, post-traumatic stress disorder, anxiety and depression. Crucially, the initial GMV in the right DLPFC can predict fatigue symptoms 3 months after infection. We provide novel evidence on the neuroanatomical basis of fatigue vulnerability and emphasize that acute fatigue is an important link between early GMV in the frontal-limbic regions and comorbid neuropsychiatric symptoms at baseline and 3 months after infection. Our findings highlight the role of the frontal-limbic system in predisposing individuals to develop post-COVID fatigue.

[This corrects the article DOI: 10.3389/fnhum.2025.1598598.].

Empathy for pain is a complex psychological process that enables us to understand the feelings of others experiencing pain. Personal pain experiences may shape our empathetic responses, though the precise relationship between empathy for pain and pain perception is not fully understood. This study investigates how firsthand pain experiences influence brain responses related to empathy for pain. We recruited 26 participants who underwent either painful or nonpainful electrical stimulation. They were then shown static pictures of hands in painful and nonpainful situations and asked to report their subjective ratings of pain empathy. Electroencephalograph activity was recorded to analyze the neural basis of their experiences. Participants who experienced painful stimulation reported higher empathy levels when viewing painful images. Electroencephalograph data revealed that painful stimulation elicited larger N1 and P2 amplitudes at the Cz electrode compared to nonpainful stimulation. It also enhanced N2 amplitudes in the frontal-central region when viewing painful pictures. Nonpainful stimulation reduced the discriminatory ability of N2 for subsequent painful and nonpainful images. Correlation analysis showed that individuals with higher pain sensitivity had greater variation in P2 responses to painful and nonpainful stimuli but less variation in N2 responses related to pain empathy. These findings suggest that experiencing pain directly may enhance brain responses to others' pain, thereby increasing levels of pain empathy. This enhancement may be influenced by individual pain sensitivity and is less pronounced in those with high pain sensitivity.

Hypertension increases risks for cognitive impairment and Alzheimer’s disease (AD). In renal patients with both hypertension and cognitive decline, via rest-state fMRI, their cerebral cortical region showed maintained cerebral blood flow (CBF), but reduced signals of blood-oxygen-level-dependent (BOLD). In mice, although CBF was unchanged, deoxycorticosterone acetate (DOCA)-salt treatment markedly reduced cerebrovascular reactivity, with altered transcriptomic pattern in cortical endothelial cells (ECs) and astrocytes, showing downregulated expression of glucose transport 1 ( GluT1 ) but upregulated metabolic reprogramming. Lipidomic analysis using prefrontal cortex (PFC) further revealed enhanced catabolism of glycerophospholipids and accumulation of free fatty acids. In the PFC of hypertensive mice, neurodegenerative alterations were observed, including reduced number of neuronal dendritic spines and more expression of phosphorylated Tau (p-Tau). Via both morphological and molecular tests, we identified that DOCA-salt hypertension was associated with significant mitochondrial injury and upregulated lysine succinylation in the PFC neurons. Upregulated lysine succinylation was largely mitochondria-located, and they were functionally enriched in gluconeogenesis-related energy metabolic pathways, the tricarboxylic acid (TCA) cycle, oxidative stress, and neurodegenerative diseases. In hypertensive mice, angiotensinogen ( Agt ) expression was markedly upregulated in most astrocytes, together with neuronal expression of Agtr1a . In cultured neuronal cells, angiotensin II (ang II) elevated mitochondrial membrane potential and ATP biosynthesis. In mice with neuronal AT 1a R knockout (AT1N), DOCA-salt failed to induce cognitive impairment. Additionally, DOCA-salt-associated reduction of acetylcholine, accumulation of p-Tau, and upregulation of lysine succinylation were not observed in AT1N mice. Direct anti-hypertensive treatment did not abolish DOCA-salt-related pathological phenotypes, and enhanced lysine succinylation was not detected in hypertension models induced by norepinephrine or L-NAME. Our data provide evidence that hypertension induced metabolic rearrangement (enhanced energy metabolism from non-glucose source and upregulated mitochondrial oxidative phosphorylation) in the neuro-vascular unit, due to downregulated glucose uptake in ECs. Increased neuronal energy consumption, via local ang II/AT 1 R signaling, further exacerbated mitochondrial stress and neurodegenerative alterations. Together, by multi-omics analysis, this study provided novel insights regarding how hypertension increases the risk for age-related cognitive impairment. Graphical Abstract

End-stage kidney disease (ESKD) is associated with cognitive impairment and affects different aspects of cortical morphometry, but where these changes converge remains unclear. Fractal dimension (FD) is used to represent cortical complexity (CC), which describes the structural complexity of the cerebral cortex by integrating different cortical morphological measures. This study aimed to investigate changes in CC in patients with ESKD prior to initiation of dialysis and to evaluate the relationship between changes in CC, cognitive performance, and uremic toxins. Forty-nine patients with ESKD naive to dialysis and 31 healthy controls (HCs) were assessed using structural magnetic resonance imaging (MRI) and cognitive tests, including evaluations of global cognitive function, memory, and executive function. Clinical laboratory blood tests were performed on all patients with ESKD, including measurement of nine uremic toxin-related indices. Cortical complexity was measured using MRI data to determine regional FD values. We estimated the association between cognitive performance, uremic toxin levels, and CC changes. Compared to HCs, patients with ESKD showed significantly lower CC in the left precuneus (p = 0.006), left middle temporal cortex (p = 0.010), and left isthmus cingulate cortex (p = 0.018). Furthermore, lower CC in the left precuneus was associated with impaired long-term delayed memory (Pearson r = 0.425, p = 0.012) in patients with ESKD. Our study suggests that regional decreases in CC are an additional characteristic of patients with ESKD naive to dialysis, related to impaired long-term memory performance. These findings may help further understand the underlying neurobiological mechanisms between brain structural changes and cognitive impairment in ESKD patients.

Depression is one of the common incidental symptoms in end-stage renal disease (ESRD) patients, empirically overlooked. Reproducible results observed that altered interregional white matter (WM) connections between depression-related brain regions (thalamus, amygdala, and prefrontal cortex (PFC)) in the human brain were closely associated with depression. Whether the depressive tendency of ESRD patients is also association with the WM connections is remains unknown. To address this problem, 56 ESRD patients before dialysis initiation and 56 healthy controls (HCs) were scanned with diffusion tensor imaging. According to the diagnostic and statistical manual of mental disorders, ESRD patients were separated into with and without depressive tendency groups. Twenty-five essential metabolites were tested in ESRD. The tractography atlas-based analysis and multiple regression analysis were implemented to gain features which could map the depressive tendency variability across ESRD. For metabolites, the levels of thrombocytes and calcium have significant differences between with and without depressive tendency groups. For WM microstructure, depressive tendency ESRD patients had abnormal WM diffusion properties along the fiber tracts of the amygdala-PFC. Compared with the features which were extracted from the group-difference of WM or metabolites, only WM features combinations (1000 bootstrap samples; 5000 permutation tests) along the fiber tract of the amygdala-PFC was a significant predictor of either with or without depressive tendency. Our findings suggested that the advanced neuroprotection may be planned before dialysis initiation, and the WM characteristics of amygdala-PFC may be a potential neuromarkers for the early diagnosis of depressive tendency in ESRD patients before dialysis initiation.

Restless legs syndrome (RLS) is common in the end-stage renal disease (ESRD) population; however, their interrelationship remains largely unclear. In the current study, we aimed to investigate the brain structure variation in ESRD patients with RLS (ERSD-RLS) and its potential relation with the severity of RLS. Diffusion tensor imaging and T1-weighted imaging were obtained from 64 ERSD-RLS and 64 matched healthy controls. Voxel-based morphometry (VBM) analysis and tractography atlas-based analysis (TABS) were used to detect the alteration of gray matter (GM) volume and white matter (WM) microstructural characterization. The corticospinal tract (CST), which is a main motor-pathway, was selected as a fiber bundle of interest in the TABS analysis. The severity of RLS was evaluated by using the International RLS Study Group scale. Lastly, a correlation analysis was performed to explore the interrelationship between RLS rating scores and brain structure measurements. For the results, ERSD-RLS showed abnormal GM volume of motor-related brain regions located in the bilateral superior frontal gyri, precentral gyrus, and putamen. Significant differences in the diffusion properties were found at the posterior limb of the internal capsule. Furthermore, the severity of RLS was only significantly associated with the diffusion properties, which was not found in the motor-related regions of GM. Our results suggest that the motor-related brain structure was altered in ERSD-RLS. The abnormal WM microstructure of the CST may serve as an imaging marker correlated with the severity of motor dysfunction in ERSD-RLS, indicating that WM neuroprotection should be considered when improving motor function in ERSD-RLS.

Background End-stage renal disease (ESRD) patients are at a substantially higher risk for developing cognitive impairment compared with the healthy population. Dialysis is an essential way to maintain the life of ESRD patients. Based on previous research, there isn’t an uncontested result whether cognition was improved or worsened during dialysis. Methods To explore the impact of dialysis treatment on cognitive performance, we recruited healthy controls (HCs), predialysis ESRD patients (predialysis group), and maintenance hemodialysis ESRD patients (HD group). All ESRD patients performed six blood biochemistry tests (hemoglobin, urea, cystatin C, Na+, K+, and parathyroid hormone). Neuropsychological tests were used to measure cognitive function. By using diffusion tensor imaging and graph-theory approaches, the topological organization of the whole-brain structural network was investigated. Generalized linear models (GLMs) were performed to investigate blood biochemistry predictors of the neuropsychological tests and the results of graph analyses in the HD group and predialysis group. Results Neuropsychological analysis showed the HD group exhibited better cognitive function than the predialysis group, but both were worse than HCs. Whole-brain graph analyses revealed that increased global efficiency and normalized shortest path length remained in the predialysis group and HD group than the HCs. Besides, a lower normalized clustering coefficient was found in the predialysis group relative to the HCs and HD group. For the GLM analysis, only the Cystatin C level was significantly associated with the average fiber length of rich club connections in the predialysis group. Conclusions Our study revealed that dialysis had a limited effect on cognitive improvement.