Background:Blood-based biomarkers have proven to be a reliable measure of the severity and outcome of traumatic brain injury(TBI)in both murine models and patients.In particular,neuronspecific enolase(NSE),neurofilame...Background:Blood-based biomarkers have proven to be a reliable measure of the severity and outcome of traumatic brain injury(TBI)in both murine models and patients.In particular,neuronspecific enolase(NSE),neurofilament light(NFL)and S100 beta(S100B)have been investigated in the clinical setting post-injury.Ethanol intoxication(EI)remains a significant comorbidity in TBI,with 30–40%of patients having a positive blood alcohol concentration post-TBI.The effect of ethanol on blood-based biomarkers for the prognosis and diagnosis of TBI remains unclear.In this study,we investigated the effect of EI on NSE,NFL and S100B and their correlation with blood–brain barrier integrity in a murine model of TBI.Methods:We used ultra-sensitive single-molecule array technology and enzyme-linked immunosorbent assay methods to measure NFL,NSE,S100B and claudin-5 concentrations in plasma 3 hours post-TBI.Results:We showed that NFL,NSE and S100B were increased at 3 hours post-TBI.Interestingly,ethanol blood concentrations showed an inverse correlation with NSE but not with NFL or S100B.Claudin-5 levels were increased post-injury but no difference was detected compared to ethanol pretreatment.The increase in claudin-5 post-TBI was correlated with NFL but not with NSE or S100B.Conclusions:Ethanol induces an effect on biomarker release in the bloodstream that is different from TBI not influenced by alcohol.This could be the basis of investigations into humans.展开更多
Dear Editor,Significant progress has been made in understanding the genetics of amyotrophic lateral sclerosis(ALS),particularly in European populations.However,a substantial proportion of familial ALS(fALS)cases remai...Dear Editor,Significant progress has been made in understanding the genetics of amyotrophic lateral sclerosis(ALS),particularly in European populations.However,a substantial proportion of familial ALS(fALS)cases remaingenetically unexplained.Emerging evidence suggests that ALS phenotypes and genetic risk factors may vary across ethnicities and regions.Investigating the genetic architecture of ALS in understudied populations could uncover new pathwaysand mechanisms contributing to motor neuron degeneration.展开更多
文摘Background:Blood-based biomarkers have proven to be a reliable measure of the severity and outcome of traumatic brain injury(TBI)in both murine models and patients.In particular,neuronspecific enolase(NSE),neurofilament light(NFL)and S100 beta(S100B)have been investigated in the clinical setting post-injury.Ethanol intoxication(EI)remains a significant comorbidity in TBI,with 30–40%of patients having a positive blood alcohol concentration post-TBI.The effect of ethanol on blood-based biomarkers for the prognosis and diagnosis of TBI remains unclear.In this study,we investigated the effect of EI on NSE,NFL and S100B and their correlation with blood–brain barrier integrity in a murine model of TBI.Methods:We used ultra-sensitive single-molecule array technology and enzyme-linked immunosorbent assay methods to measure NFL,NSE,S100B and claudin-5 concentrations in plasma 3 hours post-TBI.Results:We showed that NFL,NSE and S100B were increased at 3 hours post-TBI.Interestingly,ethanol blood concentrations showed an inverse correlation with NSE but not with NFL or S100B.Claudin-5 levels were increased post-injury but no difference was detected compared to ethanol pretreatment.The increase in claudin-5 post-TBI was correlated with NFL but not with NSE or S100B.Conclusions:Ethanol induces an effect on biomarker release in the bloodstream that is different from TBI not influenced by alcohol.This could be the basis of investigations into humans.
文摘Dear Editor,Significant progress has been made in understanding the genetics of amyotrophic lateral sclerosis(ALS),particularly in European populations.However,a substantial proportion of familial ALS(fALS)cases remaingenetically unexplained.Emerging evidence suggests that ALS phenotypes and genetic risk factors may vary across ethnicities and regions.Investigating the genetic architecture of ALS in understudied populations could uncover new pathwaysand mechanisms contributing to motor neuron degeneration.