Postoperative neurocognitive impairment is an urgent problem with global aging accelerating. The prevention and treatment of postoperative neurocognitive impairment have been widely investigated but lack effective strategies. Low-intensity pulsed ultrasound (LIPUS), a non-invasive tool, has shown an effect on neuroprotection, but whether it could attenuate the postoperative neurocognitive impairment and the underlying mechanisms remains unknown. An experimental setup for LIPUS stimulation of the hippocampus was well established. A laparotomy model in aged mice was applied, and a Morris water maze was used to assess cognitive function. RT-qPCR and western blotting were used to detect levels of Piezo1, synapse-associated proteins in the hippocampus, respectively. Immunofluorescent staining was also used to determine the neural activation and Piezo1 expression. The results showed that LIPUS increased synapse-related proteins of the hippocampus and attenuated cognitive impairment in aged mice. Meanwhile, LIPUS suppressed the overexpression of Piezo1 in the hippocampus. We further found that LIPUS promoted Calpain1 activity and increased extracellular regulated protein kinases (Erk) phosphorylation. Our results suggested that LIPUS could improve cognitive impairment and increase hippocampal synaptogenesis through the Piezo1-mediated Calpain1/ Erk pathway. LIPUS could be used as an effective physical intervention to alleviate postoperative cognitive dysfunction in the aged population.

Background: Emergence agitation (EA) is a conscious disturbance after general anesthesia in adult patients that can lead to severe respiratory or circulatory complications and serious physical injury to patients and caregivers. However, the pathophysiological mechanisms underlying EA remain unclear. The present study aimed to identify serum metabolites with significant alterations in EA patients after general anesthesia and enable inferences on their associations with EA.Methods: EA patients were identified by Richmond Agitation-Sedation Scale (RASS) ≥ + 2 among a cohort of adult patients who received elective surgery under general anesthesia in Peking University Third Hospital between 01 June 2020 and 30 December 2020. We further selected sex-, age-, and surgery type-matched non-EA control patients at a 1:1.5 ratio. Postoperative serum samples were collected from both groups of patients. An untargeted metabolic method was used to identify differences in serum metabolomic profiles between the EA patients and the non-EA patients.Results: A total of 19 EA patients and 32 matched non-EA patients were included in the study. After screening and mapping with a database, 12 metabolites showed significant postoperative alterations in EA patients compared with non-EA patients, and were mainly involved in lipid, fatty acid and amino acid metabolism pathways. Receiver operating characteristic curve analyses indicated that vanillic acid, candoxatril, tiglylglycine, 5-methoxysalicylic acid, decanoylcarnitine, and 24-epibrassinolide may be involved in EA pathogenesis after general anesthesia.Conclusion: In this study, we found differences in the serum levels of vanillic acid, candoxatril, tiglylglycine, 5-methoxysalicylic acid, decanoylcarnitine, and 24-epibrassinolide involved in fatty acid metabolism, lipid metabolism, and amino acid metabolism pathways in EA patients compared with non-EA patients, which may demonstrate an EA pathogenesis-associated molecular pattern and contribute toward better understanding of EA occurrence.

Background/Objectives: Carotid artery stenosis is a well-established risk factor for vascular cognitive impairment. Although carotid endarterectomy (CEA) reduces the risk of ischemic stroke, its effect on cognitive function remains uncertain. Most previous studies have relied on mean changes in cognitive scores and have not defined postoperative cognitive decline using patient-level thresholds for the Montreal Cognitive Assessment (MoCA). Moreover, few studies have integrated perioperative variables across baseline, intraoperative, and postoperative domains to examine heterogeneity in cognitive outcomes. We therefore defined postoperative cognitive decline using threshold-based MoCA changes and prospectively evaluated perioperative factors associated with distinct cognitive outcomes after CEA. Methods: We prospectively enrolled older patients undergoing elective CEA under general anesthesia. Of 183 patients screened, 162 were ultimately enrolled and analyzed. All patients were managed according to standardized anesthetic and surgical protocols. Preoperative clinical, laboratory, and imaging variables, intraoperative hemodynamic parameters, and postoperative clinical indicators were collected. The primary outcome was cognitive decline at discharge, defined as a decrease of ≥2 points from baseline in the MoCA score. The secondary outcome was cognitive decline at 30 days, defined as a ≥3-point decrease in the telephone MoCA (t-MoCA) score relative to the corresponding baseline domains. Results: Among the 162 enrolled patients, preoperative triglyceride level, preoperative cerebral hypoperfusion volume, surgical laterality, intraoperative mean arterial pressure (MAP) decline, and visual analogue scale (VAS) on postoperative day 1 were independently associated with early postoperative cognitive decline. A prediction model incorporating these five factors achieved an area under the curve (AUC) of 0.752 (95% CI: 0.670–0.835) for cognitive decline before discharge. For 30-day cognitive decline, the model demonstrated an AUC of 0.717 (95% CI: 0.606–0.828). All patients with complete 30-day follow-up were stratified into four cognitive trajectory subtypes, and their longitudinal cognitive changes were visualized using a Sankey diagram. Conclusions: A perioperative model incorporating metabolic, cerebral perfusion, surgical, hemodynamic, and pain-related variables may help identify patients at increased risk of cognitive decline after CEA. The trajectory analysis further reveals heterogeneous postoperative cognitive patterns, including transient, delayed, and persistent decline. These findings support individualized perioperative risk assessment and structured cognitive follow-up. However, no internal or external validation was performed, and further testing is required in larger multicenter cohorts.

Cognitive function governs human performance, but cognitive training gains rarely transfer beyond practiced tasks. Transcranial light stimulation (tLS) modulates cortical bioenergetics, offering a promising route to transcend these limits. In Experiment 1, longitudinal structural imaging data (N = 41) tracked progressive plasticity across an 11-session tLS protocol. In Experiment 2, a randomized, double-blind, 2×2 factorial trial evaluated tLS and cognitive training. Longitudinal structural imaging revealed that repeated right prefrontal tLS altered grey matter density at the target site and increased fractional anisotropy within the structurally connected right anterior thalamic radiation. Behavioral outcomes showed that combined tLS and working memory training yielded accelerated training trajectories, higher performance, and enhanced transfer to untrained tasks. Transfer toward alertness-related domains was associated with shifts in intrinsic alpha peak frequency and enhanced task-related P3b amplitudes. These findings show that tLS drives structural plasticity while accelerating task mastery and cross-task transfer.