目的探讨1990—2023年中国脊髓损伤(spinal cord injury,SCI)的流行特征和疾病负担变化趋势,对疾病负担变化进行分解分析,为SCI防控提供依据。方法基于2023年全球疾病负担研究(Global Burden of Disease,GBD)数据库数据,利用发病和伤残...目的探讨1990—2023年中国脊髓损伤(spinal cord injury,SCI)的流行特征和疾病负担变化趋势,对疾病负担变化进行分解分析,为SCI防控提供依据。方法基于2023年全球疾病负担研究(Global Burden of Disease,GBD)数据库数据,利用发病和伤残损失寿命年(years lived with disability,YLDs)指标分析1990—2023年中国SCI疾病负担的现状和变化趋势,并采用Gupta分解框架量化人口增长、人口年龄结构演变、年龄别发病率变化及疾病严重程度变化对YLDs增长的贡献。结果2023年中国SCI发病人数为23.27万例,与1990年相比增加了43.6%。1990—2023年SCI标化YLDs率呈下降趋势;标化发病率在1990—2015年逐年上升,2015年后短暂回落,2020年起再度上升,整体呈上升趋势。男性SCI疾病负担高于女性。疾病负担的年龄分布呈现向更高年龄段推移的趋势,中老年人群发病率随年龄增长而升高。跌倒是中国SCI的主要伤害原因。相比于1990年,2023年男性和女性YLDs分别增长了48.58%和41.72%,男性增长归因于人口增长、人口老龄化、年龄别发病率变化和疾病严重程度变化的比例分别为22.79%、22.69%、34.99%和-31.88%,女性分别为23.82%、26.30%、21.99%和-30.40%。结论1990—2023年人口老龄化对中国SCI疾病负担增长有突出贡献,影响疾病负担增长的首要因素在不同性别存在差异。临床干预减轻疾病严重程度是应对SCI疾病负担快速增长的关键。展开更多
After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the tim...After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the timing of interventions,combined with the limitations of current methods.To address these challenges,various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.Notably,neuromodulation has garnered considerable attention for its potential to enhance nerve regeneration,provide neuroprotection,restore neurons,and regulate the neural reorganization of circuits within the cerebral cortex and corticospinal tract.To improve the effectiveness of these interventions,the implementation of multitarget early interventional neuromodulation strategies,such as electrical and magnetic stimulation,is recommended to enhance functional recovery across different phases of nerve injury.This review concisely outlines the challenges encountered following spinal cord injury,synthesizes existing neurostimulation techniques while emphasizing neuroprotection,repair,and regeneration of impaired connections,and advocates for multi-targeted,task-oriented,and timely interventions.展开更多
Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in s...Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury.展开更多
Spinal cord injury results in permanent loss of neurological functions due to severance of neural networks.Transplantation of neural stem cells holds promise to repair disrupted connections.Yet,ensuring the survival a...Spinal cord injury results in permanent loss of neurological functions due to severance of neural networks.Transplantation of neural stem cells holds promise to repair disrupted connections.Yet,ensuring the survival and integration of neural stem cells into the host neural circuit remains a formidable challenge.Here,we investigated whether modifying the intrinsic properties of neural stem cells could enhance their integration post-transplantation.We focused on phosphatase and tensin homolog(PTEN),a well-characterized tumor suppressor known to critically regulate neuronal survival and axonal regeneration.By deleting Pten in mouse neural stem cells,we observed increased neurite outgrowth and enhanced resistance to neurotoxic environments in culture.Upon transplantation into injured spinal cords,Pten-deficient neural stem cells exhibited higher survival and more extensive rostrocaudal distribution.To examine the potential influence of partial PTEN suppression,rat neural stem cells were treated with short hairpin RNA targeting PTEN,and the PTEN knockdown resulted in significant improvements in neurite growth,survival,and neurosphere motility in vitro.Transplantation of sh PTEN-treated neural stem cells into the injured spinal cord also led to an increase in graft survival and migration to an extent similar to that of complete deletion.Moreover,PTEN suppression facilitated neurite elongation from NSC-derived neurons migrating from the lesion epicenter.These findings suggest that modifying intrinsic signaling pathways,such as PTEN,within neural stem cells could bolster their therapeutic efficacy,offering potential avenues for future regenerative strategies for spinal cord injury.展开更多
目的 分析脑机接口技术在脊髓损伤治疗领域的研究热点和发展趋势。方法 检索Web of Science核心合集数据库建库至2025年7月收录的脑机接口技术在脊髓损伤治疗领域的相关文献,采用Cite Space、VOSviewer、Tableau Desktop等工具进行可视...目的 分析脑机接口技术在脊髓损伤治疗领域的研究热点和发展趋势。方法 检索Web of Science核心合集数据库建库至2025年7月收录的脑机接口技术在脊髓损伤治疗领域的相关文献,采用Cite Space、VOSviewer、Tableau Desktop等工具进行可视化分析。结果 共纳入437篇文献,年发文量整体呈现逐渐增长趋势。发文量最多的国家是美国,发文量最多的机构是Graz University of Technology,发文量最多的作者是Gernot R Mueller-Putz,被引频次最多的作者是Jonathan R Wolpaw;brain-computer interface和artificial intelligence是领域内的高频关键词和突现词。形成神经科学和康复医学、生物医学工程、计算机科学和人工智能、神经生理学、材料科学等五大核心学科交叉融合的研究特点。结论 脑机接口技术在脊髓损伤治疗领域研究持续加速,技术融合成为核心趋势。展开更多
Traumatic spinal cord injury result in considerable and lasting functional impairments,triggering complex inflammatory and pathological events.Spinal cord scars,often metaphorically referred to as“fire barriers,”aim...Traumatic spinal cord injury result in considerable and lasting functional impairments,triggering complex inflammatory and pathological events.Spinal cord scars,often metaphorically referred to as“fire barriers,”aim to control the spread of neuroinflammation during the acute phase but later hinder axon regeneration in later stages.Recent studies have enhanced our understanding of immunomodulation,revealing that injury-associated inflammation involves various cell types and molecules with positive and negative effects.This review employs bibliometric analysis to examine the literature on inflammatory mediators in spinal cord injury,highlighting recent research and providing a comprehensive overview of the current state of research and the latest advances in studies on neuroinflammation related to spinal cord injury.We summarize the immune and inflammatory responses at different stages of spinal cord injury,offering crucial insights for future research.Additionally,we review repair strategies based on inflammatory mediators for the injured spinal cord.Finally,this review discusses the current status and future directions of translational research focused on immune-targeting strategies,including pharmaceuticals,biomedical engineering,and gene therapy.The development of a combined,precise,and multitemporal strategy for the repair of injured spinal cords represents a promising direction for future research.展开更多
文摘目的探讨1990—2023年中国脊髓损伤(spinal cord injury,SCI)的流行特征和疾病负担变化趋势,对疾病负担变化进行分解分析,为SCI防控提供依据。方法基于2023年全球疾病负担研究(Global Burden of Disease,GBD)数据库数据,利用发病和伤残损失寿命年(years lived with disability,YLDs)指标分析1990—2023年中国SCI疾病负担的现状和变化趋势,并采用Gupta分解框架量化人口增长、人口年龄结构演变、年龄别发病率变化及疾病严重程度变化对YLDs增长的贡献。结果2023年中国SCI发病人数为23.27万例,与1990年相比增加了43.6%。1990—2023年SCI标化YLDs率呈下降趋势;标化发病率在1990—2015年逐年上升,2015年后短暂回落,2020年起再度上升,整体呈上升趋势。男性SCI疾病负担高于女性。疾病负担的年龄分布呈现向更高年龄段推移的趋势,中老年人群发病率随年龄增长而升高。跌倒是中国SCI的主要伤害原因。相比于1990年,2023年男性和女性YLDs分别增长了48.58%和41.72%,男性增长归因于人口增长、人口老龄化、年龄别发病率变化和疾病严重程度变化的比例分别为22.79%、22.69%、34.99%和-31.88%,女性分别为23.82%、26.30%、21.99%和-30.40%。结论1990—2023年人口老龄化对中国SCI疾病负担增长有突出贡献,影响疾病负担增长的首要因素在不同性别存在差异。临床干预减轻疾病严重程度是应对SCI疾病负担快速增长的关键。
基金supported by the National Key Research and Development Program of China,No.2023YFC3603705(to DX)the National Natural Science Foundation of China,No.82302866(to YZ).
文摘After spinal cord injury,impairment of the sensorimotor circuit can lead to dysfunction in the motor,sensory,proprioceptive,and autonomic nervous systems.Functional recovery is often hindered by constraints on the timing of interventions,combined with the limitations of current methods.To address these challenges,various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.Notably,neuromodulation has garnered considerable attention for its potential to enhance nerve regeneration,provide neuroprotection,restore neurons,and regulate the neural reorganization of circuits within the cerebral cortex and corticospinal tract.To improve the effectiveness of these interventions,the implementation of multitarget early interventional neuromodulation strategies,such as electrical and magnetic stimulation,is recommended to enhance functional recovery across different phases of nerve injury.This review concisely outlines the challenges encountered following spinal cord injury,synthesizes existing neurostimulation techniques while emphasizing neuroprotection,repair,and regeneration of impaired connections,and advocates for multi-targeted,task-oriented,and timely interventions.
基金supported by the National Natural Science Foundation of China,Nos.82072165 and 82272256(both to XM)the Key Project of Xiangyang Central Hospital,No.2023YZ03(to RM)。
文摘Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury.
基金supported by the National Research Foundation of Korea,Nos.2021R1A2C2006110,2021M3E5D9021364,2019R1A5A2026045(to BGK)the Korea Initiative for Fostering University of Research and Innovation(KIURI)Program of the NRF funded by the MSIT(to HK),No.NRF2021M3H1A104892211(to HSK)。
文摘Spinal cord injury results in permanent loss of neurological functions due to severance of neural networks.Transplantation of neural stem cells holds promise to repair disrupted connections.Yet,ensuring the survival and integration of neural stem cells into the host neural circuit remains a formidable challenge.Here,we investigated whether modifying the intrinsic properties of neural stem cells could enhance their integration post-transplantation.We focused on phosphatase and tensin homolog(PTEN),a well-characterized tumor suppressor known to critically regulate neuronal survival and axonal regeneration.By deleting Pten in mouse neural stem cells,we observed increased neurite outgrowth and enhanced resistance to neurotoxic environments in culture.Upon transplantation into injured spinal cords,Pten-deficient neural stem cells exhibited higher survival and more extensive rostrocaudal distribution.To examine the potential influence of partial PTEN suppression,rat neural stem cells were treated with short hairpin RNA targeting PTEN,and the PTEN knockdown resulted in significant improvements in neurite growth,survival,and neurosphere motility in vitro.Transplantation of sh PTEN-treated neural stem cells into the injured spinal cord also led to an increase in graft survival and migration to an extent similar to that of complete deletion.Moreover,PTEN suppression facilitated neurite elongation from NSC-derived neurons migrating from the lesion epicenter.These findings suggest that modifying intrinsic signaling pathways,such as PTEN,within neural stem cells could bolster their therapeutic efficacy,offering potential avenues for future regenerative strategies for spinal cord injury.
文摘目的 分析脑机接口技术在脊髓损伤治疗领域的研究热点和发展趋势。方法 检索Web of Science核心合集数据库建库至2025年7月收录的脑机接口技术在脊髓损伤治疗领域的相关文献,采用Cite Space、VOSviewer、Tableau Desktop等工具进行可视化分析。结果 共纳入437篇文献,年发文量整体呈现逐渐增长趋势。发文量最多的国家是美国,发文量最多的机构是Graz University of Technology,发文量最多的作者是Gernot R Mueller-Putz,被引频次最多的作者是Jonathan R Wolpaw;brain-computer interface和artificial intelligence是领域内的高频关键词和突现词。形成神经科学和康复医学、生物医学工程、计算机科学和人工智能、神经生理学、材料科学等五大核心学科交叉融合的研究特点。结论 脑机接口技术在脊髓损伤治疗领域研究持续加速,技术融合成为核心趋势。
基金supported by the National Natural Science Foundation of China,Nos.82272470 (to GN),82072439 (to GN),81930070 (to SF)the Tianjin Health Key Discipline Special Project,No.TJWJ2022XK011 (to GN)+2 种基金the Outstanding Youth Foundation of Tianjin Medical University General Hospital,No.22ZYYJQ01 (to GN)Tianjin Key Medical Disciplines,No.TJYXZDXK-027A (to SF)National Key Research and Development Program-Stem Cells and Transformation Research,No.2019YFA0112100 (to SF)
文摘Traumatic spinal cord injury result in considerable and lasting functional impairments,triggering complex inflammatory and pathological events.Spinal cord scars,often metaphorically referred to as“fire barriers,”aim to control the spread of neuroinflammation during the acute phase but later hinder axon regeneration in later stages.Recent studies have enhanced our understanding of immunomodulation,revealing that injury-associated inflammation involves various cell types and molecules with positive and negative effects.This review employs bibliometric analysis to examine the literature on inflammatory mediators in spinal cord injury,highlighting recent research and providing a comprehensive overview of the current state of research and the latest advances in studies on neuroinflammation related to spinal cord injury.We summarize the immune and inflammatory responses at different stages of spinal cord injury,offering crucial insights for future research.Additionally,we review repair strategies based on inflammatory mediators for the injured spinal cord.Finally,this review discusses the current status and future directions of translational research focused on immune-targeting strategies,including pharmaceuticals,biomedical engineering,and gene therapy.The development of a combined,precise,and multitemporal strategy for the repair of injured spinal cords represents a promising direction for future research.
