ArticleCNS neuroscience & therapeutics2026
hUC-MSCs via β-NGF Alleviate Cognitive Impairment After Tibial Fracture Surgery by Regulating the STMN2/NMNAT2-SARM1-NF-κB Signaling Pathway.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPerioperative neurocognitive disorders (PND) are common postoperative complications, particularly in elderly patients, marked by learning and memory deficits with limited treatment options. Human umbilical cord mesenchymal stem cells (hUC-MSCs) hold promise due to their neuroprotective and immunomodulatory effects, but their underlying mechanisms remain unclear.
methodsThis study established a PND model in aged mice using tibial fracture intramedullary fixation surgery, followed by intravenous hUC-MSCs administration. Subsequently, behavioral tests, pathological examination, proteomic analysis, and other experiments were performed to verify the therapeutic effect and underlying mechanism of hUC-MSCs on PND in mice.
resultshUC-MSCs significantly improved cognitive function in PND mice, reduced hippocampal neuronal apoptosis and neuroinflammation, and restored dendritic spine density. Mechanistically, hUC-MSCs secreted β-NGF to activate the TrkA signaling pathway, upregulate STMN2 and NMNAT2 expression, and inhibit the SARM1/NF-κB pathway, thereby alleviating neuroinflammation and dendritic degeneration. Overexpression of SARM1 in the hippocampal CA1 region and β-NGF knockdown in hUC-MSCs both reversed the therapeutic effects of hUC-MSCs, confirming their critical roles.
conclusionshUC-MSCs ameliorate PND pathology through the β-NGF-mediated STMN2/NMNAT2-SARM1-NF-κB pathway, offering a novel cell-based therapeutic strategy for PND. Future research may focus on optimizing the secretory function of hUC-MSCs or developing small-molecule drugs targeting β-NGF to enhance therapeutic efficacy.
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