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INTRODUCTION: There are no reports regarding a pregnant woman with fulminant myocarditis underwent Extracorporeal Membrane Oxygenation (ECMO). Hence, we report a case of successful ECMO treatment of fulminant myocarditis puerpera. CASE PRESENTATION: A 32-year-old puerpera was admitted to our hospital with menopause for 7 months, fetal movement for 3 months and fever for 1 day. After admission, the patient's body temperature increased repeatedly, heart rate increased, and the whole process C-reactive protein increased rapidly. Considered a diagnosis of fulminant myocarditis. After antiviral and cardioprotective treatment, the heart function progressively worsened. Pregnancy was terminated, the newborn was intubated in the neonatal room for rescue after surgery, and ECMO treatment was given after the puerpera was transferred to the intensive care unit. Finally, the patient and the baby have been safely discharged from hospital. DISCUSSION: ECMO can provide cardiac and respiratory support. Fulminant myocarditis is common in children, adolescents and particularly pregnant women who had the highest mortality rate. In the pregnant woman with fulminant myocarditis described in this report, antiviral treatment only transiently improved heart function and then heart function progressively worsened. After receiving ECMO therapy, the patient's cardiac function has improved markedly. The patient was then successfully weaned from ECMO. To our knowledge, this is the first report of pregnant woman in whom ECMO was part of the treatment for fulminant myocarditis. CONCLUSION: We report a case of successful ECMO treatment of fulminant myocarditis puerpera. ECMO can be the treatment of choice for pregnant women with fulminant myocarditis.

Background: Postoperative delirium (POD) represents a serious complication following anesthesia and surgical procedures for patients undergoing surgical intervention. At present, there is no effective index to predict the occurrence of POD ,so the aim of this study was to validate whether cerebrospinal fluid (CSF) PGRN could predict the occurrence of POD.Methods: We conducted a prospective nested case-control and 1:1 matched (on age, diagnosis, American Society of Anesthesiologist’ (ASA) physical status, duration of surgery, and intraoperative blood loss) study. A total of 600 Han Chinese patients over the age of 65~ 90 who underwent unilateral total knee arthroplasty were included in the PNDABLE study from June 2020 to November 2020. POD cases and non-POD controls were selected from using Confusion Assessment Method (CAM) on the first, second, third and seventh (or before discharge) postoperative days. Delirium severity was measured by the Memorial Delirium Assessment Scale (MDAS). In the six month, cognitive function was assessed with the modified Telephone Interview for Cognitive Status (TICS-m) and the World Health Organization Quality of Life brief version (WHOQOLBREF). CSF PGRN and core biomarkers were measured by ELISA using the microplate reader. The associations of CSF PGRN levels with POD risk and CSF core biomarkers (Aβ1–42, Aβ1–40 ,T-tau and P-tau)were assessed. The effect of CSF PGRN on predicting POD occurrence was evaluated with the area under the receiver operating characteristic (ROC) curve (AUC).Results: POD incidence was 9.7% (53/545). There were significant differences in preoperative CSF PGRN concentration between POD patients and non-POD (P1–42 (β = 0.756, P < 0.001) , Aβ1–40 (β =0.637, P < 0.001) and negative associations of CSF PGRN with T-tau (β = -0.716, P < 0.001) and P-tau (β = -0.739, P < 0.001) in POD patients. The ROC curve analysis of PGRN showed that PGRN concentrations had high diagnostic value for POD.Conclusions: Aβ pathology is associated with increasing in CSF PGRN whereas Tau pathology and neurodegeneration is associated with decreasing in CSF PGRN in POD patients.CSF PGRN can predict the occurrence of POD in elderly patients．Clinical Trial Registration: www.clinicaltrials.gov, identifier ChiCTR2000033439.

BackgroundPostoperative delirium (POD) represents a serious complication following anesthesia and surgical procedures for patients undergoing surgical intervention (1). Little is known about the mechanisms underlying similarities in the core features between postoperative delirium (POD) and progranulin (PGRN)-related cognitive disorders. We herein investigated the relationship between preoperative CSF PGRN concentration and POD occurrence in the Han Chinese patients undergoing unilateral total knee arthroplasty.MethodsWe conducted an observational, prospective, and 1:1 matched (on age older than 65, the unilateral total knee arthroplasty, American Society of Anesthesiologist’ (ASA) physical status, duration of surgery, and intraoperative bleeding) case-control study. POD cases and non-POD controls were selected from the overall cohort using Confusion Assessment Method (CAM). Delirium severity was measured by the Memorial Delirium Assessment Scale (MDAS). CSF PGRN and core biomarkers were measured by ELISA using the microplate reader. The associations of CSF PGRN levels with POD risk and CSF core biomarkers were assessed.ResultsPOD incidence was 9.7% (53/545). There were significant differences in preoperative CSF PGRN concentration between POD patients and controls (P1–42 (β = -0.576, P < 0.001), Aβ1–40 (β = -0.488, P < 0.001), Aβ42/p-tau (β = -0.422, P < 0.001), and Aβ42 / T- tau (β = -0.395, P < 0.001) in POD patients. The ROC curve analysis of PGRN showed that PGRN concentrations had high diagnostic value for POD.ConclusionsCSF PGRN may be associated with the POD. Aβ pathology is associated with a decrease in CSF PGRN in the absence of tau deposition and neurodegeneration, whereas tau pathology and neurodegeneration is associated with an increase in CSF PGRN.Clinical Trial Registrationwww.clinicaltrials.gov, identifier ChiCTR2000033439.

Background Accumulating reports have suggested that α-synuclein is involved in the pathogenesis of Alzheimer’s disease (AD). As the cerebrospinal fluid (CSF) α-synuclein has been suggested as a potential biomarker of AD, this study was set out to test whether CSF α-synuclein is associated with other AD biomarkers and could predict neurodegeneration and clinical progression in non-demented elders. Methods The associations between CSF α-synuclein and other AD biomarkers were investigated at baseline in non-demented Chinese elders. The predictive values of CSF α-synuclein for longitudinal neuroimaging change and the conversion risk of non-demented elders were assessed using linear mixed effects models and multivariate Cox proportional hazard models, respectively, in the Alzheimer’s disease Neuroimaging Initiative (ADNI) database. Results The CSF α-synuclein levels correlated with AD-specific biomarkers, CSF total tau and phosphorylated tau levels, in 651 Chinese Han participants (training set). These positive correlations were replicated in the ADNI database (validation set). Using a longitudinal cohort from ADNI, the CSF α-synuclein concentrations were found to increase with disease severity. The CSF α-synuclein had high diagnostic accuracy for AD based on the “ATN” (amyloid, tau, neurodegeneration) system (A + T+ versus A − T − control) (area under the receiver operating characteristic curve, 0.84). Moreover, CSF α-synuclein predicted longitudinal hippocampus atrophy and conversion from MCI to AD dementia. Conclusions CSF α-synuclein is associated with CSF tau levels and could predict neurodegeneration and clinical progression in non-demented elders. This finding indicates that CSF α-synuclein is a potentially useful early biomarker for AD.

BackgroundAccumulating reports suggest that α-synuclein is involved in Alzheimer disease (AD) pathogenesis. Cerebrospinal fluid (CSF) α-synuclein could be a potential biomarker of AD. We sought to test whether CSF α-synuclein is associated with other AD biomarkers and could predict neurodegeneration and clinical progression in prodromal AD. MethodsAssociations were investigated between CSF α-synuclein and other AD biomarkers at baseline in prodromal AD stage Chinese elders. The predictive values of CSF α-synuclein in longitudinal change in clinical outcomes and conversion risk of prodromal AD stage subjects were assessed using linear mixed effects models and multivariate Cox proportional hazard models, respectively, in Alzheimer's disease Neuroimaging Initiative (ADNI) database.ResultsAmong individuals in prodromal AD stage, we detected that CSF α-synuclein levels correlated with AD-specific biomarkers CSF total tau and phosphorylated tau levels in 651 Chinese Han participants (training set). These positive correlations were replicated in ADNI database (validation set). Using a longitudinal cohort from ADNI, CSF α-synuclein concentrations increased with disease severity. CSF α-synuclein had high diagnostic accuracy for AD based on the “ATN” system (A+T+) vs controls (A-T-) (area under the receiver operating characteristic curve, 0.84). Moreover, CSF α-synuclein predicted longitudinal hippocampus atrophy and conversion from MCI to AD dementia.ConclusionsCSF α-synuclein is associated with CSF tau levels and could predict neurodegeneration and clinical progression in prodromal AD. This finding indicates CSF α-synuclein is a potentially useful, early biomarker for AD.

Background: The preclinical stage of Alzheimer's disease (AD) has become a key target stage for future AD prevention trials. Serum apolipoprotein, an important lipid-related factor, has been found to be involved in the pathogenesis of AD. This study was to examine whether apolipoprotein B (ApoB), apolipoprotein A-1 (ApoA1) or the ratio of ApoB and ApoA1 (ApoB/A1) were associated with early changes of cerebrospinal fluid (CSF) AD biomarkers in elderly adults with subjective cognitive decline.Methods: This study included 201 cognitive normal (CN) elderly adults and 101 participants with subjective cognitive decline (SCD) from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) database. The Kruskall-Wallis test and Chisquare test were applied in the intergroup comparisons. Multiple linear regression models were used to examine the cross-sectional associations of serum ApoB, ApoA1 and ApoB/A1 levels with CSF AD-related biomarkers.Results: Compared with the control group, SCD participants with significant AD biological characteristics had lower ApoB levels. In the total participants, higher level of serum ApoB was associated with increases in CSF Aβ42 (p = 0.0009) and Aβ42/40 (p = 0.0038) as well as decreases in CSF t-tau/Aβ42 (p < 0.0001) and p-tau/Aβ42 (p < 0.0001), independent of APOEɛ4 status. In the further subgroup analysis, these associations were much more significant in the SCD participants. In addition, higher levels of serum ApoB were also found associated with decreases in CSF t-tau (p = 0.0224), p-tau (p = 0.0086) and Aβ40 (p = 0.0297) in the SCD subgroup. Furthermore, we found that these protective associations between serum ApoB and CSF AD core biomarkers were much more significant in the overweight participants. Results showed no association between ApoA1 and all CSF biomarkers in either total participants or subgroups. Conclusions: This study is the first to find protective associations of serum ApoB, but not ApoA1, with CSF AD core biomarkers in elderly adults, and these associations were more significant in SCD individuals. This finding indicated that ApoB may play a protective role in the preclinical stage of AD. Identifying the underlying mechanisms may contribute to the discovery of new pathogenic mechanisms and therapeutic targets.

Background The preclinical stage of Alzheimer's disease (AD) has become a key target stage for future AD prevention trials. Serum apolipoprotein, an important lipid-related factor, has been found to be involved in the pathogenesis of AD. This study was to examine whether apolipoprotein B (ApoB), apolipoprotein A-1 (ApoA1) or the ratio of ApoB and ApoA1 (ApoB/A1) were associated with early changes of cerebrospinal fluid (CSF) AD biomarkers in elderly adults with subjective cognitive decline. Methods This study included 201 cognitive normal (CN) elderly adults and 101 participants with subjective cognitive decline (SCD) from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) database. The Kruskall-Wallis test and Chisquare test were applied in the intergroup comparisons. Multiple linear regression models were used to examine the cross-sectional associations of serum ApoB, ApoA1 and ApoB/A1 levels with CSF AD-related biomarkers. Results Compared with the control group, SCD participants with significant AD biological characteristics had lower ApoB levels. In the total participants, higher level of serum ApoB was associated with increases in CSF Aβ42 (p = 0.0009) and Aβ42/40 (p = 0.0038) as well as decreases in CSF t-tau/Aβ42 (p < 0.0001) and p-tau/Aβ42 (p < 0.0001), independent of APOEɛ4 status. In the further subgroup analysis, these associations were much more significant in the SCD participants. In addition, higher levels of serum ApoB were also found associated with decreases in CSF t-tau (p = 0.0224), p-tau (p = 0.0086) and Aβ40 (p = 0.0297) in the SCD subgroup. Furthermore, we found that these protective associations between serum ApoB and CSF AD core biomarkers were much more significant in the overweight participants. Results showed no association between ApoA1 and all CSF biomarkers in either total participants or subgroups. Conclusions This study is the first to find protective associations of serum ApoB, but not ApoA1, with CSF AD core biomarkers in elderly adults, and these associations were more significant in SCD individuals. This finding indicated that ApoB may play a protective role in the preclinical stage of AD. Identifying the underlying mechanisms may contribute to the discovery of new pathogenic mechanisms and therapeutic targets.

BackgroundThe preclinical stage of Alzheimer's disease (AD) has become a key target stage for future AD prevention trials. Plasma apolipoprotein, an important lipid-related factor, has been found to be involved in the pathogenesis of AD. This study was to examine whether apolipoprotein B (ApoB), apolipoprotein A-1 (ApoA1) or the ratio of ApoB and ApoA1 (ApoB/A1) were associated with early changes of cerebrospinal fluid (CSF) AD biomarkers in elderly adults with subjective cognitive decline.MethodsThis study finally included 201 cognitive normal (CN) elderly adults and 101 participants with subjective cognitive decline (SCD) from the Chinese Alzheimer’s Biomarker and Lifestyle (CABLE) database. The One-way analysis of variance, t-test, Kruskall-Wallis test and Chisquare test were applied in the intergroup comparisons. Multiple linear regression models were used to examine the cross-sectional associations of plasma ApoB, ApoA1 and ApoB/A1 levels with CSF AD-related biomarkers.ResultsCompared with the control group, SCD participants with significant AD biological characteristics had lower ApoB levels. In the total participants, higher level of plasma ApoB was associated with increases in CSF Aβ42 (p = 0.0009) and Aβ42/40 (p = 0.0038) as well as decreases in CSF t-tau/Aβ42 (p < 0.0001) and p-tau/Aβ42 (p < 0.0001), independent of APOEɛ4 status. In the further subgroup analysis, these associations were much more significant in the SCD participants. In addition, higher levels of plasma ApoB were also found associated with decreases in CSF t-tau (p = 0.0224), p-tau (p = 0.0086) and Aβ40 (p = 0.0297) in the SCD subgroup. Furthermore, we found that these protective associations between plasma ApoB and CSF AD core biomarkers were much more significant in the overweight participants. Results showed no association between ApoA1 and all CSF biomarkers in either total participants or subgroups. ConclusionsThis study is the first to find protective associations of plasma ApoB, but not ApoA1, with CSF AD core biomarkers in elderly adults, and these associations were more significant in SCD individuals. This finding indicated that ApoB may play a protective role in the preclinical stage of AD. Identifying the underlying mechanisms may contribute to the discovery of new pathogenic mechanisms and therapeutic targets.

Background: Sex hormone-binding globulin (SHBG) in plasma has been found to be significantly elevated in subjects with AD. We aimed to investigate whether plasma SHBG was associated with AD biomarkers and could predict neurodegeneration and clinical progression in prodromal AD.Methods: The study tested the cross-sectional relationship between plasma SHBG and CSF AD biomarkers in 707 non-demented adults. Next, the longitudinal influences of plasma SHBG at baseline on dynamic changes of CSF Aβ42, hippocampus volume, brain metabolism, and cognition were explored in 448 non-demented adults from the Alzheimer’s disease Neuroimaging Initiative (ADNI). Finally, the influence of plasma SHBG on the risk of incident AD was explored. Results: This study included 707 participants (mean [SD] age, 62.5 [10.5] years, 416 [58.8%] female) from CABLE and 448 from ADNI-1 (mean [SD] age, 74.8 [7.2] years, 166 [37.5%] female). A positive correlation was found for SHBG levels in plasma and CSF (p = 2.12 × 10 -10, r = 0.44). Cross-sectional analyses indicated that individuals with higher plasma SHBG had lower levels of CSF Aβ42 (p < 0.005), after adjusting for age, gender, education, APOE4 allele, and cognitive scores. The longitudinal data showed that higher levels of plasma SHBG contribute to accelerated CSF Aβ42 decrease (p < 0.0005), brain metabolism decline (p < 0.05), hippocampus atrophy (p < 0.01), cognitive decline (p < 0.01), and higher risk of AD dementia (p < 0.05).Conclusions: Plasma SHBG is associated with CSF Aβ42 levels and could predict neurodegeneration and clinical progression in prodromal AD. This finding indicates plasma SHBG is a potentially useful, early biomarker for AD.