Background: Patients in minimally conscious state (MCS) exist measurable evidence of consciousness. The frontal lobe is a crucial part of the brain that encodes abstract information and is closely related to the conscious state. We hypothesized that the disturbance of the frontal functional network exists in MCS patients.Methods: We collected the resting-state functional near-infrared spectroscopy (fNIRS) data of fifteen MCS patients and sixteen age- and gender-matched healthy controls (HC). The Coma Recovery Scale-Revised (CRS-R) scale of MCS patients was also composed. The topology of the frontal functional network was analyzed in two groups.Results: Compared with HC, the MCS patients showed widely disrupted functional connectivity in the frontal lobe, especially in the frontopolar area and right dorsolateral prefrontal cortex. Moreover, the MCS patients displayed lower clustering coefficient, global efficiency, local efficiency, and higher characteristic path length. In addition, the nodal clustering coefficient and nodal local efficiency in the left frontopolar area and right dorsolateral prefrontal cortex were significantly reduced in MCS patients. Furthermore, the nodal clustering coefficient and nodal local efficiency in the right dorsolateral prefrontal cortex were positively correlated to auditory subscale scores.Conclusion: This study reveals that MCS patients’ frontal functional network is synergistically dysfunctional. And the balance between information separation and integration in the frontal lobe is broken, especially the local information transmission in the prefrontal cortex. These findings help us to understand the pathological mechanism of MCS patients better.

A typical enriched environment (EE), which combines physical activity and social interaction, has been proven to mitigate cognitive impairment caused by chronic cerebral hypoperfusion (CCH). However, it remains unclear how the different components of EE promote cognitive recovery after CCH. This study stripped out the different components of EE into physical environmental enrichment (PE) and social environmental enrichment (SE), and compared the neuroprotective effects of PE, SE and typical EE (PSE) in CCH. The results of novel object recognition and Morris water maze tests showed that PE, SE, and PSE improved cognitive function in CCH rats. Additionally, Nissl and TUNEL staining revealed that three EEs reduced neuronal loss in the hippocampus. PSE exhibited superior neuroprotective and functional improvement effects compared to PE and SE, while there was no significant difference between PE and SE. Furthermore, three EEs reduced lipid peroxidation in the hippocampus with decreasing the levels of MDA and increasing the activities of SOD and GSH. The expression of SLC7A11 and GPX4 was increased, while the level of p53 was reduced in three EEs. This suggested that three EEs inhibited ferroptosis by maintaining the redox homeostasis in the hippocampus. Three EEs reduced the levels of IL-β, TNF-α, and IL-6, thereby inhibiting neuroinflammation. Additionally, Western blotting and immunofluorescence results indicated that three EEs also inhibited the TLR4/MyD88/p38MAPK signaling pathway. These findings collectively demonstrated that the three EEs alleviated hippocampal ferroptosis and neuroinflammation in CCH rats, thereby reducing neuronal loss, which might be associated with the inhibition of the TLR4/MyD88/p38MAPK signaling pathway. Moreover, the study results supported that it is only through the combination of physical exercise and social interaction that the optimal neuroprotective effects can be achieved. These findings provided valuable insights for the prevention and treatment of vascular cognitive impairment.

Introduction Poststroke cognitive impairment is a common complication in stroke survivors, seriously affecting their quality of life. Therefore, it is crucial to improve cognitive function of patients who had a stroke. Transcranial direct current stimulation (tDCS) and transcutaneous auricular vagus nerve stimulation (taVNS) are non-invasive, safe treatments with great potential to improve cognitive function in poststroke patients. However, further improvements are needed in the effectiveness of a single non-invasive brain stimulation technique for cognitive rehabilitation. This study protocol aims to investigate the effect and neural mechanism of the combination of tDCS and taVNS on cognitive function in patients who had a stroke. Methods and analysis In this single-centre, prospective, parallel, randomised controlled trial, a total of 66 patients with poststroke cognitive impairment will be recruited and randomly assigned (1:1:1) to the tDCS group, the taVNS group and the combination of tDCS and taVNS group. Each group will receive 30 min of treatment daily, five times weekly for 3 weeks. Primary clinical outcome is the Montreal Cognitive Assessment. Secondary clinical outcomes include the Mini-Mental State Examination, Stroop Colour Word Test, Trail Marking Test, Symbol Digit Modalities Test and Modified Barthel Index. All clinical outcomes, functional MRI and diffusion tensor imaging will be measured at preintervention and postintervention. Ethics and dissemination The trial has been approved by the Ethics Committee of the First Affiliated Hospital of Yangtze University (approval no: KY202390). The results will be submitted for publication in peer-reviewed journals or at scientific conferences. Trial registration number ChiCTR2300076632.

Stroke represents a leading cause of non-traumatic prolonged disorders of consciousness (pDoC). Given the prefrontal cortex's critical role in consciousness, this study aimed to explore the abnormalities in the prefrontal network in post-stroke pDoC patients. Using resting-state functional near-infrared spectroscopy (fNIRS), we acquired data from 21 post-stroke pDoC patients and 19 age- and gender-matched healthy controls (HC). Based on the Coma Recovery Scale-Revised, patients were classified into 12 with minimally conscious state (MCS) and 9 with unresponsive wakefulness syndrome (UWS). We analyzed and compared functional connectivity and topological properties of the prefrontal network across groups. Compared to HCs, the pDoC group exhibited extensively weakened functional connectivity and disrupted network topology, as evidenced by a lower clustering coefficient (Cp), reduced local efficiency (Eloc), global efficiency (Eg) and a longer characteristic path length (Lp). Reductions in key nodal metrics which including nodal clustering coefficient (NCp), nodal efficiency (Ne), and degree centrality (DC) were also observed across several prefrontal regions. In the direct comparison between patient subgroups, the MCS group demonstrated significantly stronger functional connectivity within the right premotor and supplementary motor cortex (PreM & SMA_R) than the UWS group, but conversely, showed weaker connectivity within the left frontopolar area (FPA_L). Consequently, assessing prefrontal network integrity with portable fNIRS holds promise for identifying potential biomarkers to diagnose and monitor post-stroke prolonged disorders of consciousness.

Neuroplasticity plays a pivotal role in post‐stroke recovery, and Angelica sinensis polysaccharide has demonstrated neuroprotective properties. This study investigated the neuroprotective effects of low‐molecular‐weight Angelica sinensis polysaccharide (LMW‐ASP) in a rat middle cerebral artery occlusion/reperfusion (MCAO/R) model. Structural characterization revealed that LMW‐ASP (3.9 kDa), containing a pyranose ring and uronic acid, was a heteropolysaccharide that comprised fucose, galactosamine hydrochloride, rhamnose, arabinose, glucosamine hydrochloride, galactose, glucose, xylose, mannose, galacturonic acid, and glucuronic acid (0.007:0.003:0.057:0.209:0.009:0.284:0.303:0.006:0.032:0.083:0.007). Post‐stroke administration of LMW‐ASP (50 mg/kg) significantly improved body weight and neurological functions after MCAO/R. Moreover, microtubule‐associated protein‐2 expression was notably higher in the LMW‐ASP group than in the model group ( p < 0.01). Furthermore, Golgi‐Cox staining confirmed that LMW‐ASP increased the number of dendritic intersections ( p < 0.05 for 90–120, 180, and 200 μm; p < 0.001 for 70 and 80 μm), the number of terminal branches ( p < 0.01), the number of branch points ( p < 0.01), and the density of basal dendritic spines ( p < 0.05). Finally, transmission electron microscopy revealed an increase in the number of synapses ( p < 0.001) and presynaptic vesicles ( p < 0.001) in the LMW‐ASP group. These results suggest that LMW‐ASP is a potential pharmaceutical therapeutic approach for stroke recovery that enhances neuroplasticity.