Proteomics is a powerful tool that can be used to elucidate the underlying mechanisms of diseases and identify new biomarkers.Therefore,it may also be helpful for understanding the detailed pathological mechanism of t...Proteomics is a powerful tool that can be used to elucidate the underlying mechanisms of diseases and identify new biomarkers.Therefore,it may also be helpful for understanding the detailed pathological mechanism of traumatic brain injury(TBI).In this study,we performed Tandem Mass Tag-based quantitative analysis of cortical proteome profiles in a mouse model of TBI.Our results showed that there were 302 differentially expressed proteins in TBI mice compared with normal mice 7 days after injury.Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that these differentially expressed proteins were predominantly involved in inflammatory responses,including complement and coagulation cascades,as well as chemokine signaling pathways.Subsequent transcription factor analysis revealed that the inflammation-related transcription factors NF-κB1,RelA,IRF1,STAT1,and Spi1 play pivotal roles in the secondary injury that occurs after TBI,which further corroborates the functional enrichment for inflammatory factors.Our results suggest that inflammation-related proteins and inflammatory responses are promising targets for the treatment of TBI.展开更多
Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently understood.As potent anti-i...Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently understood.As potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet known.In the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action.In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization.Lipopolysaccharide,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were administered.RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone.The Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our hypothesis.High-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain injury.Thus dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in vivo.Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury.Additionally,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway.Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia,which plays an antiinflammatory role.In contrast,inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury.Dexamethasone may exe rt its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway.展开更多
Poststro ke cognitive impairment is a major secondary effect of ischemic stroke in many patients;however,few options are available for the early diagnosis and treatment of this condition.The aims of this study were to...Poststro ke cognitive impairment is a major secondary effect of ischemic stroke in many patients;however,few options are available for the early diagnosis and treatment of this condition.The aims of this study were to(1)determine the specific relationship between hypoxic andα-synuclein during the occur of poststroke cognitive impairment and(2)assess whether the serum phosphorylatedα-synuclein level can be used as a biomarker for poststro ke cognitive impairment.We found that the phosphorylatedα-synuclein level was significantly increased and showed pathological aggregation around the cerebral infa rct area in a mouse model of ischemic stroke.In addition,neuronalα-synuclein phosphorylation and aggregation were observed in the brain tissue of mice subjected to chronic hypoxia,suggesting that hypoxia is the underlying cause ofα-synuclein-mediated pathology in the brains of mice with ischemic stroke.Serum phosphorylatedα-synuclein levels in patients with ischemic stroke were significantly lower than those in healt hy subjects,and were positively correlated with cognition levels in patients with ischemic stroke.Furthermore,a decrease in serum high-density lipoprotein levels in stroke patie nts was significantly correlated with a decrease in phosphorylatedα-synuclein levels.Although ischemic stroke mice did not show significant cognitive impairment or disrupted lipid metabolism 14 days after injury,some of them exhibited decreased cognitive function and reduced phosphorylatedα-synuclein levels.Taken together,our results suggest that serum phosphorylatedα-synuclein is a potential biomarker for poststroke cognitive impairment.展开更多
Cerebral amyloid angiopathy(CAA)is a small vessel disease of the brain characterized by the progressive deposition of amyloid-β(Aβ)plaques in the walls of cerebral blood vessels.It presents with a subtle course and ...Cerebral amyloid angiopathy(CAA)is a small vessel disease of the brain characterized by the progressive deposition of amyloid-β(Aβ)plaques in the walls of cerebral blood vessels.It presents with a subtle course and sudden onset,and currently,there are no specific therapeutic interventions available.Accurate diagnosis of CAA could enable targeted interventions in the early stages of the disease,potentially mitigating the disease’s effects.Herein,we review the primary imaging biomarkers used in the diagnosis of CAA,including their mechanisms,imaging characteristics,and significance.We also provide an interpretation of the latest version(v2.0)of the Boston criteria,which are commonly used in the clinical diagnosis of CAA.Additionally,this study introduces various positron emission tomography(PET)tracers for CAA and reviews their application values in the diagnosis of CAA.展开更多
Single-cell transcriptome sequencing has been a rapidly developing and powerful biological tool in recent years,and it plays a vital role in describing tissue development,cell heterogeneity,stress response,etc.Cerebro...Single-cell transcriptome sequencing has been a rapidly developing and powerful biological tool in recent years,and it plays a vital role in describing tissue development,cell heterogeneity,stress response,etc.Cerebrovascular disease is one of the leading causes affecting human health in the world.Thus,it is important to understand the characteristics of cerebrovascular structure,function,and environmental response.Notably,single-cell transcriptome sequencing provides deeper insights into cerebrovascular research in health and disease states.This article will briefly introduce the basic structure and function of cerebrovascular endothelial cells(ECs),summarize the current research and new findings on cerebrovascular ECs at the single-cell transcriptome level,and discuss the challenges in this field.展开更多
Ischemic stroke is characterized by high incidence,high mortality,and high disability and is the primary cause of death and disability among adults in China.Endogenous neural stem cells(NSCs)are a group of cells that ...Ischemic stroke is characterized by high incidence,high mortality,and high disability and is the primary cause of death and disability among adults in China.Endogenous neural stem cells(NSCs)are a group of cells that have the potential to self-renew and differentiate into functional nerve cells.Under normal circumstances,NSCs are in a quiet state.When the body is subjected to specific stimulation or injury,NSCs can be activated,proliferate,migrate to the damaged site,and differentiate into functional nerve cells to repair the injured tissue.NSCs induced by ischemic stimulation have limited regenerative capacity and cannot completely restore damaged tissues.Exogenous NSC transplantation has some effect.However,it is limited by the low survival rate of transplanted NSCs,immune rejection,ethics,and risk of tumor formation.Therefore,it is necessary to study further the strategies and mechanisms of endogenous NSC activation to promote nerve function repair after stroke.This article reviews recent advancements in drug therapy,hypoxic/ischemic conditioning,Chinese medicine,and rehabilitation strategies for NSC treatment.Furthermore,it explores new strategies and mechanisms developed recently,offering innovative plans and ideas to enhance clinical stroke treatment.展开更多
Objective:To systematically review the etiology of anterior choroidal artery(AChA)infarction.Methods:A systematic literature search up to May 11,2024,for AChA infarction with its etiology.Epidemiologic and clinical da...Objective:To systematically review the etiology of anterior choroidal artery(AChA)infarction.Methods:A systematic literature search up to May 11,2024,for AChA infarction with its etiology.Epidemiologic and clinical data of patients,anatomic distribution of the lesions,and etiologic classification of AChA infarction were extracted.Results:A total of 1007 individual patient data was included(967 from retrospective clinical studies and 40 from case reports).Among the clinical research,patients’mean age was 64.7.There were 62.24%of male and 37.76%of female patients.Hypertension(66.04%)was the most common risk factor for patients with AChA infarction.Dyslipidemia(32.92%),diabetes mellitus(30.93%),and smoking(26.54%)were also common risk factors.Moreover,the posterior limb of the internal capsule was the most frequently affected structure.Undetermined etiology(n=173,38.02%),according to the trial of org 10172 in acute stroke treatment(TOAST)etiological classification,was the most common etiology,followed by small vessel disease(n=117,25.71%),large artery atherosclerosis(n=84,18.46%),and cardioembolism(n=63,13.85%).Furthermore,eighteen strokes were caused by other determined etiologies(3.96%).Conclusions:Undetermined etiology was the most common etiology of AChA infarction.Hypertension,dyslipidemia,diabetes mellitus,and smoking were common risk factors for patients with AChA infarction.It is necessary to prevent the risk factors.展开更多
Objective:To evaluate the basic appearance and variation of the venous sinuses and veins in healthy individuals.Methods:Prospectively-recruited healthy volunteers completed a questionnaire and underwent magnetic reson...Objective:To evaluate the basic appearance and variation of the venous sinuses and veins in healthy individuals.Methods:Prospectively-recruited healthy volunteers completed a questionnaire and underwent magnetic resonance imaging plus contrast-enhanced magnetic resonance venography(CE-MRV)to measure their sinus diameters.Anatomical variations of cerebral venous sinuses were evaluated.Results:Fifty-eight individuals were included.The mean diameter of the left transverse sinus(LTS)(5.37±1.35 mm)was significantly smaller than that of the right transverse sinus(RTS)(6.65±1.57 mm)(P<0.001),and the average discrepancy was 19.2%.RTS dominance was noted in 55.1%of cases.Four superior sagittal sinus(SSS)anatomical variations were found.Type A was the most common and was present in 43 participants(74.1%).The SSS preferentially drained into the RTS in 32 patients(55.2%),and arachnoid granulation was observed in the transverse sinus(TS)and SSS in patients.According to our reclassification combined with Osborn’s previous research,we found that the SSS commonly drained into the RTS and that the straight sinus(StS)branched into both TSs.Conclusions:A 19%difference between the LTS and RTS provides a threshold for TS lateral dominance instead of a TS abnormality.Clinicians and radiologists should not ignore the influence of acquired pathology when the SSS drains in a non-RTS-dominant manner.Anatomical variations of the torcular herophili are frequent;the most commonly observed was the StS branching into both TSs,with the SSS draining into the RTS.展开更多
Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability,inhibit free radicals,and reduce cerebrospinal fluid p...Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability,inhibit free radicals,and reduce cerebrospinal fluid production.According to the latest guidelines for the treatment of traumatic brain injury in the United States,high-dose glucocorticoids cause neurological damage.To investigate the reason why high-dose glucocorticoids after traumatic brain injury exhibit harmful effect,rat controlled cortical impact models of traumatic brain injury were established.At 1 hour and 2 days after surgery,rat models were intraperitoneally administered dexamethasone 10 mg/kg.The results revealed that 31 proteins were significantly upregulated and 12 proteins were significantly downregulated in rat models of traumatic brain injury after dexamethasone treatment.The Ingenuity Pathway Analysis results showed that differentially expressed proteins were enriched in the mitochondrial dysfunction pathway and synaptogenesis signaling pathway.Western blot analysis and immunohistochemistry results showed that Ndufv2,Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model group.These findings suggest that dexamethasone may promote a compensatory increase in complex I subunits(Ndufs2 and Ndufv2),increase the expression of mitochondrial enzyme Maob,and upregulate synaptic-transmission-related protein Gria3.These changes may be caused by nerve injury after traumatic brain injury treatment by dexamethasone.The study was approved by Institutional Ethics Committee of Beijing Neurosurgical Institute(approval No.201802001)on June 6,2018.展开更多
The development of brain-computer interfaces(BCIs)has established a new communication channel between the brain and external devices for information transmission that requires no muscular signals[1].BCIs have been pre...The development of brain-computer interfaces(BCIs)has established a new communication channel between the brain and external devices for information transmission that requires no muscular signals[1].BCIs have been preliminarily studied to improve motor functions in patients with severe motor disabilities,especially lock-in syndrome.At present,the application of BCIs has been extensively validated.展开更多
Background Deep brain stimulation(DBS)has been preliminarily applied to treat patients with disorders of consciousness(DoCs).The study aimed to determine whether DBS was effective for treating patients with DoC and id...Background Deep brain stimulation(DBS)has been preliminarily applied to treat patients with disorders of consciousness(DoCs).The study aimed to determine whether DBS was effective for treating patients with DoC and identify factors related to patients’outcomes.Methods Data from 365 patients with DoCs who were consecutively admitted from 15 July 2011 to 31 December 2021 were retrospectively analysed.Multivariate regression and subgroup analysis were performed to adjust for potential confounders.The primary outcome was improvement in consciousness at 1 year.Results An overall improvement in consciousness at 1 year was achieved in 32.4%(12/37)of the DBS group compared with 4.3%(14/328)of the conservative group.After full adjustment,DBS significantly improved consciousness at 1 year(adjusted OR 11.90,95%CI 3.65-38.46,p<0.001).There was a significant treatment×follow up interaction(H=14.99,p<0.001).DBS had significantly better effects in patients with minimally conscious state(MCS)compared with patients with vegetative state/unresponsive wakefulness syndrome(p for interaction<0.001).A nomogram based on age,state of consciousness,pathogeny and duration of DoCs indicated excellent predictive performance(c-index=0.882).Conclusions DBS was associated with better outcomes in patients with DoC,and the effect was likely to be significantly greater in patients with MCS.DBS should be cautiously evaluated by nomogram preoperatively,and randomised controlled trials are still needed.展开更多
This review discusses the functions of blood vessels such as coagulation,regulation,immunity,endocrinology,and nerve conduction from a new perspective and suggests that hypoxia plays a common role in the changes in va...This review discusses the functions of blood vessels such as coagulation,regulation,immunity,endocrinology,and nerve conduction from a new perspective and suggests that hypoxia plays a common role in the changes in vascular function in various cardiovascular and cerebrovascular diseases.Therefore,it is oxygen therapy regulation may be a particularly beneficial means by which to regulate vascular function due to its low risk of harm and ease of implementation.Further,the authors have identified a link between vascular function and diseases caused by endogenous hypoxia and analyzed it in depth.The potential effects of hypoxia regulation schemes such as hyperxia,hyperoxic-hypoxia alternations,hypoxia preconditioning,and intermittent hypoxia on vascular function are also discussed,and we present theoretical support for targeted vascular therapy.展开更多
Early or ultra-early pharmacological thrombolysis together with mechanical thrombectomy are key treatments for ischemic stroke,and both are aimed at vascular recanalization and improved collateral circulation.While th...Early or ultra-early pharmacological thrombolysis together with mechanical thrombectomy are key treatments for ischemic stroke,and both are aimed at vascular recanalization and improved collateral circulation.While these methods enhance tissue perfusion in the ischemic penumbra,they also trigger complex neurotoxic reactions,including apoptosis,acidosis,ion imbalance,oxidative stress,and pyroptosis,exacerbating cerebral ischemia-reperfusion injury(CIRI).Pyroptosis,a recently discovered form of programmed cell death driven by inflammation,plays a significant role in neuronal death during CIRI.This study reviews the regulatory mechanisms of pyroptosis in CIRI.展开更多
Objective:Early and accurate identification of large vessel occlusion(LVO)acute ischemic stroke(AIS)patients is critically important for stroke management.Practicable scales with simple items can facilitate prehospita...Objective:Early and accurate identification of large vessel occlusion(LVO)acute ischemic stroke(AIS)patients is critically important for stroke management.Practicable scales with simple items can facilitate prehospital paramedics distinguishing LVO-AIS patients with high efficiency and help to avoid unnecessary and costly delays.The current study aims to develop a screening tool to predict AIS-LVO patients based on prehospital available data.Method:A total of 251 suspected stroke patients who were transported to the emergency department of our hospital via emergency medical services were consecutively enrolled from August,2020 to January,2022.Data including demographic information,medical history,clinical manifestations,and vital signs were collected.A multivariate logistic regression model was developed based on statistically significant variables selected from univariate analysis.Result:Forty-two patients(16.7%)were diagnosed as LVO-AIS based on imaging validation at admission.A comprehensive model was developed with past medical history factors such as atrial fibrillation and coronary heart disease,vital signs such as systolic blood pressure,and prominent symptoms and signs such as gaze palsy,facial paralysis,and dysarthria.The model showed better diagnostic performance in terms of area under the receiver operating characteristic curves(0.884,95%CI,0.830-0.939),which was higher than other common prehospital prediction scales such as the Face,Arm,Speech,Time test(FAST),the Field Assessment Stroke Triage for Emergency Destination(FAST-ED)scale,and the Gaze-Face-Arm-Speech-Time test(G-FAST).Calibration curve analysis,decision curve analysis,and clinical impact curve analysis further validated the reliability,net benefit,and potential clinical impact of the prediction model,respectively.Conclusion:We conducted a prediction model based on prehospital accessible factors including past history of atrial fibrillation and coronary heart disease,systolic blood pressure,and signs such as gaze palsy,facial palsy,and dysarthria.The prediction model showed good diagnostic power and accuracy for identification of the high-risk patients with LVO and may become an effective tool for the LVO recognition in prehospital settings.Future studies are warranted to refine and validate the model further in order to enhance the accuracy and objectivity of clinical judgments.展开更多
Objective To determine the association of carotid plaque features with collateral circulation status in elderly patients with moderate to severe carotid stenosis.Methods Elderly patients(>60 years)with moderate to ...Objective To determine the association of carotid plaque features with collateral circulation status in elderly patients with moderate to severe carotid stenosis.Methods Elderly patients(>60 years)with moderate to severe carotid stenosis were recruited and categorized into good and poor collateral circulation groups,and underwent magnetic resonance imaging and computed tomography imaging.The carotid plaque features including lipid-rich necrotic core,intraplaque hemorrhage,calcification,and fibrous cap rupture(FCR)were evaluated,and maximum wall thickness,normalized wall index(NWI),and luminal stenosis were measured.The association between these variables and collateral circulation status was analyzed.Results Of the 97 patients(78 males,mean age:69.0±6.1 years),19(19.6%)had poor collaterals.The poor collateral group had a significantly higher NWI(93.7%±5.0%vs.89.0%±7.9%,P=0.011),a greater extent of stenosis(80.0%±11.4%vs.75.3%±9.4%,P=0.036)and FCR(84.2%vs.55.1%,P=0.020)compared with good collateral group.Carotid NWI(OR=3.83,95%CI:1.36–10.82,P=0.011)and more FCR(OR=6.77,95%CI:1.35–33.85,P=0.020)were associated with poor collateral circulation after adjustment for the confounding factors.The combination of NWI,FCR,systolic blood pressure,and triglycerides had the highest area-under-the-curve(AUC=0.85)for detection of poor collaterals.Conclusions Carotid plaque features,specifically NWI and FCR,are independently associated with poor collateral circulation,and the combination of carotid plaque features and traditional risk factors has a stronger predictive value for poor collateral circulation than plaque features alone.展开更多
As a common and serious psychiatric disorder,depression significantly affects psychosocial functioning and quality of life.However,the mechanism of depression is still enigmatic and perplexing,which limits its precise...As a common and serious psychiatric disorder,depression significantly affects psychosocial functioning and quality of life.However,the mechanism of depression is still enigmatic and perplexing,which limits its precise and effective therapeutic methods.Recent studies demonstrated that neuroinflammation activation plays an important role in the pathophysiology of depression.In this respect,high mobility group box 1(HMGB1)may be a possible signaling inducer of neuroinflammation and can be a potential mechanistic and therapeutic target for depression.Herein,we review recent studies on the mechanistic and therapeutic targets of HMGB1 in depression and propose potential perspectives on this topic.展开更多
Translational medicine in neurodegenerative and neurovascular diseases is approaching a breakthrough point.Recent years have led to dramatic progress in both experimental and clinical research.Based on a much better a...Translational medicine in neurodegenerative and neurovascular diseases is approaching a breakthrough point.Recent years have led to dramatic progress in both experimental and clinical research.Based on a much better and continuously increasing understanding of disease mechanisms,progression and pathophysiology,new therapies with an improved translational potential to protect tissue either against acute or chronic degeneration and even approaches potentially capable of repairing damaged brain tissue are emerging.展开更多
Primary and secondary neurodegeneration is a pathological hallmark of numerous central nervous system(CNS)disorders.Although many mechanisms leading to neurodegeneration are well understood,previous approaches aiming ...Primary and secondary neurodegeneration is a pathological hallmark of numerous central nervous system(CNS)disorders.Although many mechanisms leading to neurodegeneration are well understood,previous approaches aiming at providing protection from neurodegeneration were often futile.A potential explanation may be that recent research discovered additional pathomechanisms leading to neurodegeneration.Thus,simply targeting single neurodegenerative mechanisms may only have minor therapeutic impact.Addressing multiple neurodegenerative mechanisms may be a more viable strategy.Moreover,the restoration of lost brain tissue turned out to be a very complex endeavor.1 Despite making some initial progress with the use of biocompatible scaffolds and hydrogels.展开更多
Background and purpose The inflammatory response mediated by microglia/macrophages is closely related to cerebral ischaemia/reperfusion injury.Wild-type p53-induced protein phosphatase 1(Wip1),a serine/threonine phosp...Background and purpose The inflammatory response mediated by microglia/macrophages is closely related to cerebral ischaemia/reperfusion injury.Wild-type p53-induced protein phosphatase 1(Wip1),a serine/threonine phosphatase,is expressed in various tissues.A growing number of reports have suggested that Wip1 is a negative regulator of inflammation in peripheral tissue;however,its role in the central nervous system(CNS)remains unclear.This study aimed to clarify whether Wip1 can inhibit CNS inflammation by regulating microglia/macrophage functions after ischaemic injury.Methods A model of middle cerebral artery occlusion and reperfusion was established in mice.CNS inflammation was simulated by lipopolysaccharide treatment of primary microglia.Laser speckle imaging was used to monitor regional cerebral blood flow.Behavioural outcomes were assessed with a TreadScan gait analysis system.TTC staining was used to evaluate the infarct volume,and western blotting and immunofluorescence staining were applied to detect the phenotypical transformation of microglia.ELISA was performed to detect the levels of inflammatory factors.Results Wip1 expression was increased after ischaemia/reperfusion.Wip1-knockout(KO)mice displayed more severe brain injury than wild-type mice,as indicated by aggravated motor dysfunction,greater brain infarct volumes and higher expression of inflammatory cytokines(interleukin-6 and tumour necrosis factor alpha)in the brain.We also found that Wip1 depletion increased microglial/macrophage activation in both in vitro and in vivo models,which all showed activation of microglia/macrophages.Lentivirus-Ppm1d reversed the injury induced by Wip1-KO.Conclusions Our results suggest that Wip1 may inhibit neuroinflammation by inhibiting microglial/macrophage activation after brain ischaemia/reperfusion injury.展开更多
BACKGROUND Cerebral microbleeds(CMBs)may increase the risk of future intracerebral hemorrhage and ischemic stroke.However,It is unclear whether antiplatelet medication is associated with CMBs.This study aimed to inves...BACKGROUND Cerebral microbleeds(CMBs)may increase the risk of future intracerebral hemorrhage and ischemic stroke.However,It is unclear whether antiplatelet medication is associated with CMBs.This study aimed to investigate the association between antiplatelet medication and CMBs in a community-based stroke-free population.METHODS In this cross-sectional study,stroke-free participants aged 18-85 years were recruited from a community in Beijing,China.Demographic,clinical,and antiplatelet medication data were collected through a questionnaire,and all participants underwent blood tests and brain magnetic resonance imaging at 3.0T.The presence,count,and location of CMBs were evaluated using susceptibility-weighted imaging.The association between antiplatelet medication and the presence of CMBs was analyzed using multivariable logistic regression.The associations between antiplatelet medication and CMBs by location(lobar,deep brain or infratentorial,and mixed regions)were also analyzed using multinomial logistic regression.A linear regression analysis was conducted to determine the association between antiplatelet medication and the log-transformed number of CMBs.RESULTS Of the 544 participants(mean age:58.65±13.66 years,217 males),119 participants(21.88%)had CMBs,and 64 participants(11.76%)used antiplatelet medication.Antiplatelet medication was found to be associated with CMBs at any location[odds ratio(OR)=2.39,95%CI:1.24-4.58]and lobar region(OR=2.83,95%CI:1.36-5.86),but not with the number of CMBs(β=0.14,95%CI:-0.21-0.48).Among antiplatelet medications,aspirin use was found to be associated with any CMB(OR=3.17,95%CI:1.49-6.72)and lobar CMBs(OR=3.61,95%CI:1.57-8.26).CONCLUSIONS Antiplatelet medication was associated with CMBs in stroke-free participants,particularly lobar CMBs.Among antiplatelet medications,aspirin use was associated with any CMB and lobar CMBs.Our findings suggest that it might be essential to optimize the management of antiplatelet medication in the stroke-free population with a higher burden of vascular risk factors to reduce the potential risk of CMBs.展开更多
基金supported by the National Natural Science Foundation of China,No. 81771327a grant for the Platform Construction of Basic Research and Clinical Translation of Nervous System Injury,China,No. PXM2020_026280_000002 (both to BYL)
文摘Proteomics is a powerful tool that can be used to elucidate the underlying mechanisms of diseases and identify new biomarkers.Therefore,it may also be helpful for understanding the detailed pathological mechanism of traumatic brain injury(TBI).In this study,we performed Tandem Mass Tag-based quantitative analysis of cortical proteome profiles in a mouse model of TBI.Our results showed that there were 302 differentially expressed proteins in TBI mice compared with normal mice 7 days after injury.Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that these differentially expressed proteins were predominantly involved in inflammatory responses,including complement and coagulation cascades,as well as chemokine signaling pathways.Subsequent transcription factor analysis revealed that the inflammation-related transcription factors NF-κB1,RelA,IRF1,STAT1,and Spi1 play pivotal roles in the secondary injury that occurs after TBI,which further corroborates the functional enrichment for inflammatory factors.Our results suggest that inflammation-related proteins and inflammatory responses are promising targets for the treatment of TBI.
基金supported by research grants from the Ningbo Science and Technology Plan Project,No.2022Z143hezuo(to BL)the National Natural Science Foundation of China,No.82201520(to XD)。
文摘Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently understood.As potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet known.In the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action.In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization.Lipopolysaccharide,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were administered.RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone.The Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our hypothesis.High-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain injury.Thus dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in vivo.Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury.Additionally,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway.Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia,which plays an antiinflammatory role.In contrast,inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury.Dexamethasone may exe rt its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway.
基金supported by the Scientific Research Project of China Rehabilitation Research Center,No.2021zx-23the National Natural Science Foundation of China,No.32100925the Beijing Nova Program,No.Z211100002121038。
文摘Poststro ke cognitive impairment is a major secondary effect of ischemic stroke in many patients;however,few options are available for the early diagnosis and treatment of this condition.The aims of this study were to(1)determine the specific relationship between hypoxic andα-synuclein during the occur of poststroke cognitive impairment and(2)assess whether the serum phosphorylatedα-synuclein level can be used as a biomarker for poststro ke cognitive impairment.We found that the phosphorylatedα-synuclein level was significantly increased and showed pathological aggregation around the cerebral infa rct area in a mouse model of ischemic stroke.In addition,neuronalα-synuclein phosphorylation and aggregation were observed in the brain tissue of mice subjected to chronic hypoxia,suggesting that hypoxia is the underlying cause ofα-synuclein-mediated pathology in the brains of mice with ischemic stroke.Serum phosphorylatedα-synuclein levels in patients with ischemic stroke were significantly lower than those in healt hy subjects,and were positively correlated with cognition levels in patients with ischemic stroke.Furthermore,a decrease in serum high-density lipoprotein levels in stroke patie nts was significantly correlated with a decrease in phosphorylatedα-synuclein levels.Although ischemic stroke mice did not show significant cognitive impairment or disrupted lipid metabolism 14 days after injury,some of them exhibited decreased cognitive function and reduced phosphorylatedα-synuclein levels.Taken together,our results suggest that serum phosphorylatedα-synuclein is a potential biomarker for poststroke cognitive impairment.
基金funded by the National Natural Science Foundation of China(82372018 and 81701753)The Beijing Natural Science Foundation(7222299)+1 种基金Beijing Medical Authority Cultivation Program(PX2022035)Medical Innovation Capability Improvement Plan of Capital Medical University(12300124).
文摘Cerebral amyloid angiopathy(CAA)is a small vessel disease of the brain characterized by the progressive deposition of amyloid-β(Aβ)plaques in the walls of cerebral blood vessels.It presents with a subtle course and sudden onset,and currently,there are no specific therapeutic interventions available.Accurate diagnosis of CAA could enable targeted interventions in the early stages of the disease,potentially mitigating the disease’s effects.Herein,we review the primary imaging biomarkers used in the diagnosis of CAA,including their mechanisms,imaging characteristics,and significance.We also provide an interpretation of the latest version(v2.0)of the Boston criteria,which are commonly used in the clinical diagnosis of CAA.Additionally,this study introduces various positron emission tomography(PET)tracers for CAA and reviews their application values in the diagnosis of CAA.
文摘Single-cell transcriptome sequencing has been a rapidly developing and powerful biological tool in recent years,and it plays a vital role in describing tissue development,cell heterogeneity,stress response,etc.Cerebrovascular disease is one of the leading causes affecting human health in the world.Thus,it is important to understand the characteristics of cerebrovascular structure,function,and environmental response.Notably,single-cell transcriptome sequencing provides deeper insights into cerebrovascular research in health and disease states.This article will briefly introduce the basic structure and function of cerebrovascular endothelial cells(ECs),summarize the current research and new findings on cerebrovascular ECs at the single-cell transcriptome level,and discuss the challenges in this field.
基金supported by the National Key R&D Program of China(2022YFC3602401)the Beijing Natural Science Foundation(JQ22020)the National Natural Science Foundation of China(82274401).
文摘Ischemic stroke is characterized by high incidence,high mortality,and high disability and is the primary cause of death and disability among adults in China.Endogenous neural stem cells(NSCs)are a group of cells that have the potential to self-renew and differentiate into functional nerve cells.Under normal circumstances,NSCs are in a quiet state.When the body is subjected to specific stimulation or injury,NSCs can be activated,proliferate,migrate to the damaged site,and differentiate into functional nerve cells to repair the injured tissue.NSCs induced by ischemic stimulation have limited regenerative capacity and cannot completely restore damaged tissues.Exogenous NSC transplantation has some effect.However,it is limited by the low survival rate of transplanted NSCs,immune rejection,ethics,and risk of tumor formation.Therefore,it is necessary to study further the strategies and mechanisms of endogenous NSC activation to promote nerve function repair after stroke.This article reviews recent advancements in drug therapy,hypoxic/ischemic conditioning,Chinese medicine,and rehabilitation strategies for NSC treatment.Furthermore,it explores new strategies and mechanisms developed recently,offering innovative plans and ideas to enhance clinical stroke treatment.
文摘Objective:To systematically review the etiology of anterior choroidal artery(AChA)infarction.Methods:A systematic literature search up to May 11,2024,for AChA infarction with its etiology.Epidemiologic and clinical data of patients,anatomic distribution of the lesions,and etiologic classification of AChA infarction were extracted.Results:A total of 1007 individual patient data was included(967 from retrospective clinical studies and 40 from case reports).Among the clinical research,patients’mean age was 64.7.There were 62.24%of male and 37.76%of female patients.Hypertension(66.04%)was the most common risk factor for patients with AChA infarction.Dyslipidemia(32.92%),diabetes mellitus(30.93%),and smoking(26.54%)were also common risk factors.Moreover,the posterior limb of the internal capsule was the most frequently affected structure.Undetermined etiology(n=173,38.02%),according to the trial of org 10172 in acute stroke treatment(TOAST)etiological classification,was the most common etiology,followed by small vessel disease(n=117,25.71%),large artery atherosclerosis(n=84,18.46%),and cardioembolism(n=63,13.85%).Furthermore,eighteen strokes were caused by other determined etiologies(3.96%).Conclusions:Undetermined etiology was the most common etiology of AChA infarction.Hypertension,dyslipidemia,diabetes mellitus,and smoking were common risk factors for patients with AChA infarction.It is necessary to prevent the risk factors.
基金supported by the National Natural Science Foundation of China(82027802)the Pharmaceutical Collaboration Project of the Beijing Science and Technology Commission(Z181100001918026)the Talents Gathering Project of Xuanwu Hospital,Capital Medical University.
文摘Objective:To evaluate the basic appearance and variation of the venous sinuses and veins in healthy individuals.Methods:Prospectively-recruited healthy volunteers completed a questionnaire and underwent magnetic resonance imaging plus contrast-enhanced magnetic resonance venography(CE-MRV)to measure their sinus diameters.Anatomical variations of cerebral venous sinuses were evaluated.Results:Fifty-eight individuals were included.The mean diameter of the left transverse sinus(LTS)(5.37±1.35 mm)was significantly smaller than that of the right transverse sinus(RTS)(6.65±1.57 mm)(P<0.001),and the average discrepancy was 19.2%.RTS dominance was noted in 55.1%of cases.Four superior sagittal sinus(SSS)anatomical variations were found.Type A was the most common and was present in 43 participants(74.1%).The SSS preferentially drained into the RTS in 32 patients(55.2%),and arachnoid granulation was observed in the transverse sinus(TS)and SSS in patients.According to our reclassification combined with Osborn’s previous research,we found that the SSS commonly drained into the RTS and that the straight sinus(StS)branched into both TSs.Conclusions:A 19%difference between the LTS and RTS provides a threshold for TS lateral dominance instead of a TS abnormality.Clinicians and radiologists should not ignore the influence of acquired pathology when the SSS drains in a non-RTS-dominant manner.Anatomical variations of the torcular herophili are frequent;the most commonly observed was the StS branching into both TSs,with the SSS draining into the RTS.
基金This study was supported by the National Natural Science Foundation of China,No.81771327(to BYL)the Platform Construction of Basic Research and Clinical Translation of Nervous System Injury,China,No.PXM2020_026280_000002(to BYL)the Scientific Research and Cultivation Fund of the Beijing Neurosurgical Institute,China,No.2020002(to FN).
文摘Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability,inhibit free radicals,and reduce cerebrospinal fluid production.According to the latest guidelines for the treatment of traumatic brain injury in the United States,high-dose glucocorticoids cause neurological damage.To investigate the reason why high-dose glucocorticoids after traumatic brain injury exhibit harmful effect,rat controlled cortical impact models of traumatic brain injury were established.At 1 hour and 2 days after surgery,rat models were intraperitoneally administered dexamethasone 10 mg/kg.The results revealed that 31 proteins were significantly upregulated and 12 proteins were significantly downregulated in rat models of traumatic brain injury after dexamethasone treatment.The Ingenuity Pathway Analysis results showed that differentially expressed proteins were enriched in the mitochondrial dysfunction pathway and synaptogenesis signaling pathway.Western blot analysis and immunohistochemistry results showed that Ndufv2,Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model group.These findings suggest that dexamethasone may promote a compensatory increase in complex I subunits(Ndufs2 and Ndufv2),increase the expression of mitochondrial enzyme Maob,and upregulate synaptic-transmission-related protein Gria3.These changes may be caused by nerve injury after traumatic brain injury treatment by dexamethasone.The study was approved by Institutional Ethics Committee of Beijing Neurosurgical Institute(approval No.201802001)on June 6,2018.
基金supported by the National Natural Science Foundation of China(81600919)the Beijing Nova Program(Z181100006218050).
文摘The development of brain-computer interfaces(BCIs)has established a new communication channel between the brain and external devices for information transmission that requires no muscular signals[1].BCIs have been preliminarily studied to improve motor functions in patients with severe motor disabilities,especially lock-in syndrome.At present,the application of BCIs has been extensively validated.
基金the following funding sources:the National Natural Science Foundation of China(81600919)Beijing Municipal Science and Technology Commission(Z161100000516165 and Z171100001017162)Beijing Nova Program(Z181100006218050).
文摘Background Deep brain stimulation(DBS)has been preliminarily applied to treat patients with disorders of consciousness(DoCs).The study aimed to determine whether DBS was effective for treating patients with DoC and identify factors related to patients’outcomes.Methods Data from 365 patients with DoCs who were consecutively admitted from 15 July 2011 to 31 December 2021 were retrospectively analysed.Multivariate regression and subgroup analysis were performed to adjust for potential confounders.The primary outcome was improvement in consciousness at 1 year.Results An overall improvement in consciousness at 1 year was achieved in 32.4%(12/37)of the DBS group compared with 4.3%(14/328)of the conservative group.After full adjustment,DBS significantly improved consciousness at 1 year(adjusted OR 11.90,95%CI 3.65-38.46,p<0.001).There was a significant treatment×follow up interaction(H=14.99,p<0.001).DBS had significantly better effects in patients with minimally conscious state(MCS)compared with patients with vegetative state/unresponsive wakefulness syndrome(p for interaction<0.001).A nomogram based on age,state of consciousness,pathogeny and duration of DoCs indicated excellent predictive performance(c-index=0.882).Conclusions DBS was associated with better outcomes in patients with DoC,and the effect was likely to be significantly greater in patients with MCS.DBS should be cautiously evaluated by nomogram preoperatively,and randomised controlled trials are still needed.
文摘This review discusses the functions of blood vessels such as coagulation,regulation,immunity,endocrinology,and nerve conduction from a new perspective and suggests that hypoxia plays a common role in the changes in vascular function in various cardiovascular and cerebrovascular diseases.Therefore,it is oxygen therapy regulation may be a particularly beneficial means by which to regulate vascular function due to its low risk of harm and ease of implementation.Further,the authors have identified a link between vascular function and diseases caused by endogenous hypoxia and analyzed it in depth.The potential effects of hypoxia regulation schemes such as hyperxia,hyperoxic-hypoxia alternations,hypoxia preconditioning,and intermittent hypoxia on vascular function are also discussed,and we present theoretical support for targeted vascular therapy.
文摘Early or ultra-early pharmacological thrombolysis together with mechanical thrombectomy are key treatments for ischemic stroke,and both are aimed at vascular recanalization and improved collateral circulation.While these methods enhance tissue perfusion in the ischemic penumbra,they also trigger complex neurotoxic reactions,including apoptosis,acidosis,ion imbalance,oxidative stress,and pyroptosis,exacerbating cerebral ischemia-reperfusion injury(CIRI).Pyroptosis,a recently discovered form of programmed cell death driven by inflammation,plays a significant role in neuronal death during CIRI.This study reviews the regulatory mechanisms of pyroptosis in CIRI.
基金sponsored by National Natural Science Foundation of China(No.82101389 and 81971114)Beijing Nova Program(No.20230484286)General Project of Science and Technology of Beijing Municipal Education Commission(No.KM202110025018).
文摘Objective:Early and accurate identification of large vessel occlusion(LVO)acute ischemic stroke(AIS)patients is critically important for stroke management.Practicable scales with simple items can facilitate prehospital paramedics distinguishing LVO-AIS patients with high efficiency and help to avoid unnecessary and costly delays.The current study aims to develop a screening tool to predict AIS-LVO patients based on prehospital available data.Method:A total of 251 suspected stroke patients who were transported to the emergency department of our hospital via emergency medical services were consecutively enrolled from August,2020 to January,2022.Data including demographic information,medical history,clinical manifestations,and vital signs were collected.A multivariate logistic regression model was developed based on statistically significant variables selected from univariate analysis.Result:Forty-two patients(16.7%)were diagnosed as LVO-AIS based on imaging validation at admission.A comprehensive model was developed with past medical history factors such as atrial fibrillation and coronary heart disease,vital signs such as systolic blood pressure,and prominent symptoms and signs such as gaze palsy,facial paralysis,and dysarthria.The model showed better diagnostic performance in terms of area under the receiver operating characteristic curves(0.884,95%CI,0.830-0.939),which was higher than other common prehospital prediction scales such as the Face,Arm,Speech,Time test(FAST),the Field Assessment Stroke Triage for Emergency Destination(FAST-ED)scale,and the Gaze-Face-Arm-Speech-Time test(G-FAST).Calibration curve analysis,decision curve analysis,and clinical impact curve analysis further validated the reliability,net benefit,and potential clinical impact of the prediction model,respectively.Conclusion:We conducted a prediction model based on prehospital accessible factors including past history of atrial fibrillation and coronary heart disease,systolic blood pressure,and signs such as gaze palsy,facial palsy,and dysarthria.The prediction model showed good diagnostic power and accuracy for identification of the high-risk patients with LVO and may become an effective tool for the LVO recognition in prehospital settings.Future studies are warranted to refine and validate the model further in order to enhance the accuracy and objectivity of clinical judgments.
基金supported by the National Natural Science Foundation of China(No.81771825)Peking University Third Hospital(BYSY2015013)+1 种基金Beijing Municipal Science and Technology Commission(D171100003017003)Ministry of Science and Technology of China(2017 YFC1307904).
文摘Objective To determine the association of carotid plaque features with collateral circulation status in elderly patients with moderate to severe carotid stenosis.Methods Elderly patients(>60 years)with moderate to severe carotid stenosis were recruited and categorized into good and poor collateral circulation groups,and underwent magnetic resonance imaging and computed tomography imaging.The carotid plaque features including lipid-rich necrotic core,intraplaque hemorrhage,calcification,and fibrous cap rupture(FCR)were evaluated,and maximum wall thickness,normalized wall index(NWI),and luminal stenosis were measured.The association between these variables and collateral circulation status was analyzed.Results Of the 97 patients(78 males,mean age:69.0±6.1 years),19(19.6%)had poor collaterals.The poor collateral group had a significantly higher NWI(93.7%±5.0%vs.89.0%±7.9%,P=0.011),a greater extent of stenosis(80.0%±11.4%vs.75.3%±9.4%,P=0.036)and FCR(84.2%vs.55.1%,P=0.020)compared with good collateral group.Carotid NWI(OR=3.83,95%CI:1.36–10.82,P=0.011)and more FCR(OR=6.77,95%CI:1.35–33.85,P=0.020)were associated with poor collateral circulation after adjustment for the confounding factors.The combination of NWI,FCR,systolic blood pressure,and triglycerides had the highest area-under-the-curve(AUC=0.85)for detection of poor collaterals.Conclusions Carotid plaque features,specifically NWI and FCR,are independently associated with poor collateral circulation,and the combination of carotid plaque features and traditional risk factors has a stronger predictive value for poor collateral circulation than plaque features alone.
文摘As a common and serious psychiatric disorder,depression significantly affects psychosocial functioning and quality of life.However,the mechanism of depression is still enigmatic and perplexing,which limits its precise and effective therapeutic methods.Recent studies demonstrated that neuroinflammation activation plays an important role in the pathophysiology of depression.In this respect,high mobility group box 1(HMGB1)may be a possible signaling inducer of neuroinflammation and can be a potential mechanistic and therapeutic target for depression.Herein,we review recent studies on the mechanistic and therapeutic targets of HMGB1 in depression and propose potential perspectives on this topic.
基金Support of the State of Rio de Janeiro,Grant/Award Numbers:202.751/2018,210.825/2021,201.460/2022National Institute of Health,Grant/Award Number:NIH/NINDS R03NS123733Deutsche Forschungsgemeinschaft,Grant/Award Number:CA 2642/1-1。
文摘Translational medicine in neurodegenerative and neurovascular diseases is approaching a breakthrough point.Recent years have led to dramatic progress in both experimental and clinical research.Based on a much better and continuously increasing understanding of disease mechanisms,progression and pathophysiology,new therapies with an improved translational potential to protect tissue either against acute or chronic degeneration and even approaches potentially capable of repairing damaged brain tissue are emerging.
基金Academy of Medical Sciences,Grant/Award Number:NAFIR111010NIH/NIDA,Grant/Award Number:R01DA056739。
文摘Primary and secondary neurodegeneration is a pathological hallmark of numerous central nervous system(CNS)disorders.Although many mechanisms leading to neurodegeneration are well understood,previous approaches aiming at providing protection from neurodegeneration were often futile.A potential explanation may be that recent research discovered additional pathomechanisms leading to neurodegeneration.Thus,simply targeting single neurodegenerative mechanisms may only have minor therapeutic impact.Addressing multiple neurodegenerative mechanisms may be a more viable strategy.Moreover,the restoration of lost brain tissue turned out to be a very complex endeavor.1 Despite making some initial progress with the use of biocompatible scaffolds and hydrogels.
基金This study was funded by Incubation foundation of Capital Medical University(PYZ2018061)Nature and Sciences Foundation of China(81430044,81974183,81930054,82072104).
文摘Background and purpose The inflammatory response mediated by microglia/macrophages is closely related to cerebral ischaemia/reperfusion injury.Wild-type p53-induced protein phosphatase 1(Wip1),a serine/threonine phosphatase,is expressed in various tissues.A growing number of reports have suggested that Wip1 is a negative regulator of inflammation in peripheral tissue;however,its role in the central nervous system(CNS)remains unclear.This study aimed to clarify whether Wip1 can inhibit CNS inflammation by regulating microglia/macrophage functions after ischaemic injury.Methods A model of middle cerebral artery occlusion and reperfusion was established in mice.CNS inflammation was simulated by lipopolysaccharide treatment of primary microglia.Laser speckle imaging was used to monitor regional cerebral blood flow.Behavioural outcomes were assessed with a TreadScan gait analysis system.TTC staining was used to evaluate the infarct volume,and western blotting and immunofluorescence staining were applied to detect the phenotypical transformation of microglia.ELISA was performed to detect the levels of inflammatory factors.Results Wip1 expression was increased after ischaemia/reperfusion.Wip1-knockout(KO)mice displayed more severe brain injury than wild-type mice,as indicated by aggravated motor dysfunction,greater brain infarct volumes and higher expression of inflammatory cytokines(interleukin-6 and tumour necrosis factor alpha)in the brain.We also found that Wip1 depletion increased microglial/macrophage activation in both in vitro and in vivo models,which all showed activation of microglia/macrophages.Lentivirus-Ppm1d reversed the injury induced by Wip1-KO.Conclusions Our results suggest that Wip1 may inhibit neuroinflammation by inhibiting microglial/macrophage activation after brain ischaemia/reperfusion injury.
基金supported by the National Key Research and Development Program of the Ministry of Science and Technology of China(2017YFC 1307702)the Capital’s Funds for Health Improvement and Research(No.2020-1-2041).
文摘BACKGROUND Cerebral microbleeds(CMBs)may increase the risk of future intracerebral hemorrhage and ischemic stroke.However,It is unclear whether antiplatelet medication is associated with CMBs.This study aimed to investigate the association between antiplatelet medication and CMBs in a community-based stroke-free population.METHODS In this cross-sectional study,stroke-free participants aged 18-85 years were recruited from a community in Beijing,China.Demographic,clinical,and antiplatelet medication data were collected through a questionnaire,and all participants underwent blood tests and brain magnetic resonance imaging at 3.0T.The presence,count,and location of CMBs were evaluated using susceptibility-weighted imaging.The association between antiplatelet medication and the presence of CMBs was analyzed using multivariable logistic regression.The associations between antiplatelet medication and CMBs by location(lobar,deep brain or infratentorial,and mixed regions)were also analyzed using multinomial logistic regression.A linear regression analysis was conducted to determine the association between antiplatelet medication and the log-transformed number of CMBs.RESULTS Of the 544 participants(mean age:58.65±13.66 years,217 males),119 participants(21.88%)had CMBs,and 64 participants(11.76%)used antiplatelet medication.Antiplatelet medication was found to be associated with CMBs at any location[odds ratio(OR)=2.39,95%CI:1.24-4.58]and lobar region(OR=2.83,95%CI:1.36-5.86),but not with the number of CMBs(β=0.14,95%CI:-0.21-0.48).Among antiplatelet medications,aspirin use was found to be associated with any CMB(OR=3.17,95%CI:1.49-6.72)and lobar CMBs(OR=3.61,95%CI:1.57-8.26).CONCLUSIONS Antiplatelet medication was associated with CMBs in stroke-free participants,particularly lobar CMBs.Among antiplatelet medications,aspirin use was associated with any CMB and lobar CMBs.Our findings suggest that it might be essential to optimize the management of antiplatelet medication in the stroke-free population with a higher burden of vascular risk factors to reduce the potential risk of CMBs.
