In view of the paucity of data on cerebrospinal fluid (CSF) biomarkers in Chinese patients, we evaluated the validity of tau, phosphorylated tau 181 (p-tau-181), amyloid β 42 (Aβ42), and Aβ40 proteins in Chinese patients with Alzheimer’s disease (AD). We recruited 24 patients with AD, 12 nondemented controls, and 12 patients with non-AD dementia. We found the CSF levels of Aβ42, tau, p-tau, Aβ42–tau, and Aβ42–p-tau ratios, except the Aβ40 protein level, were significantly different among the 3 groups of patients. Patients with AD had higher levels of CSF tau and p-tau but lower levels of Aβ42 proteins, Aβ42–tau, and Aβ42–p-tau ratios than the nondemented controls. In the diagnosis of AD versus nondementia, the sensitivity and specificity of the ratios of Aβ42–tau and Aβ42–p-tau were 96% and 83% versus 92% and 83%, respectively. Only the Aβ42–p-tau ratio showed satisfactory sensitivity and specificity in the diagnosis of AD versus other dementia.

In view of the paucity of data on cerebrospinal fluid (CSF) biomarkers in Chinese patients, we evaluated the validity of tau, phosphorylated tau 181 (p-tau-181), amyloid β 42 (Aβ42), and Aβ40 proteins in Chinese patients with Alzheimer's disease (AD). We recruited 24 patients with AD, 12 nondemented controls, and 12 patients with non-AD dementia. We found the CSF levels of Aβ42, tau, p-tau, Aβ42-tau, and Aβ42-p-tau ratios, except the Aβ40 protein level, were significantly different among the 3 groups of patients. Patients with AD had higher levels of CSF tau and p-tau but lower levels of Aβ42 proteins, Aβ42-tau, and Aβ42-p-tau ratios than the nondemented controls. In the diagnosis of AD versus nondementia, the sensitivity and specificity of the ratios of Aβ42-tau and Aβ42-p-tau were 96% and 83% versus 92% and 83%, respectively. Only the Aβ42-p-tau ratio showed satisfactory sensitivity and specificity in the diagnosis of AD versus other dementia.

Cerebrospinal fluid (CSF) concentrations of amyloid β peptides ending at positions 42 and 40 (Aβ42 and Aβ40, respectively), and total tau (tTau) protein were measured by ELISA in order to compare their accuracy in discriminating patients with Alzheimer’s disease (AD, n=22), non-Alzheimer dementia (nAD, n=11) and control subjects (CON, n=35). As compared to the other groups, the concentrations of Aβ42 and tTau were decreased (P<0.001) and increased (P<0.001) in AD, respectively, while Aβ40 did not differ significantly among the groups. Receiver operating characteristic (ROC) analysis was performed to define cut-off values for maximized sensitivity and specificity. For all groups compared the Aβ peptide ratio 42/40 classified more patients correctly, as compared to the concentration of Aβ42 alone: AD versus controls, 94 and 86.7%; AD versus nAD, 90 and 85% and AD versus nAD plus controls, 90.8 and 87%, respectively. The percentage of correctly classified patients was further improved when the Aβ ratio was combined with the analysis of the tTau concentration. Presence of the apolipoprotein E ε4 allele, age or degree of mental disability did not significantly influence the parameters studied.

The goal of this study is to investigate the value of tau phosphorylated at threonine 181 (P-tau181P) in the Alzheimer’s disease (AD) cerebrospinal fluid (CSF) biomarker panel for differential dementia diagnosis in autopsy confirmed AD and non-AD patients. The study population consisted of 140 autopsy confirmed AD and 77 autopsy confirmed non-AD dementia patients. CSF concentrations of amyloid-β peptide of 42 amino acids (Aβ1–42), total tau protein (T-tau), and P-tau181P were determined with single analyte ELISA-kits (INNOTEST®, Fujirebio, Ghent, Belgium). Diagnostic accuracy was assessed through receiver operating characteristic (ROC) curve analyses to obtain area under the curve (AUC) values and to define optimal cutoff values to discriminate AD from pooled and individual non-AD groups. ROC curve analyses were only performed on biomarkers and ratios that differed significantly between the groups. Pairwise comparison of AUC values was performed by means of DeLong tests. The Aβ1–42/P-tau181P ratio (AUC = 0.770) performed significantly better than Aβ1–42 (AUC = 0.677, P = 0.004), T-tau (AUC = 0.592, P < 0.001), and Aβ1–42/T-tau (AUC = 0.678, P = 0.001), while P-tau181P (AUC = 0.720) performed significantly better than T-tau (AUC = 0.592, P < 0.001) to discriminate between AD and the pooled non-AD group. When comparing AD and the individual non-AD diagnoses, Aβ1–42/P-tau181P (AUC = 0.894) discriminated AD from frontotemporal dementia significantly better than Aβ1–42 (AUC = 0.776, P = 0.020) and T-tau (AUC = 0.746, P = 0.004), while P-tau181P/T-tau (AUC = 0.958) significantly improved the differentiation between AD and Creutzfeldt-Jakob disease as compared to Aβ1–42 (AUC = 0.688, P = 0.004), T-tau (AUC = 0.874, P = 0.040), and Aβ1–42/P-tau181P (AUC = 0.760, P = 0.003). In conclusion, this study demonstrates P-tau181P is an essential component of the AD CSF biomarker panel, and combined assessment of Aβ1–42, T-tau, and P-tau181P renders, to present date, the highest diagnostic power to discriminate between AD and non-AD dementias.

In a large multicentre sample of cognitively normal subjects, as a function of age, gender and APOE genotype, we studied the frequency of abnormal cerebrospinal fluid levels of Alzheimer&#39;s disease biomarkers including: total tau, phosphorylated tau and amyloid-β1-42. Fifteen cohorts from 12 different centres with either enzyme-linked immunosorbent assays or Luminex® measurements were selected for this study. Each centre sent nine new cerebrospinal fluid aliquots that were used to measure total tau, phosphorylated tau and amyloid-β1-42 in the Gothenburg laboratory. Seven centres showed a high correlation with the new Gothenburg measurements; therefore, 10 cohorts from these centres are included in the analyses here (1233 healthy control subjects, 40-84 years old). Amyloid-β amyloid status (negative or positive) and neurodegeneration status (negative or positive) was established based on the pathological cerebrospinal fluid Alzheimer&#39;s disease cut-off values for cerebrospinal ...

Situated at the crossroads between Northeast Africa, the Mediterranean, the Near East and the Indian Ocean, ancient Egypt was a strategic pathway that facilitated contacts and the circulation of peoples, products and ideas across these vast regions. Sometimes the monarchy took the initiative in these contacts, whereas in other cases, mobile populations, local leaders, itinerant merchants and independent individuals fulfilled such a role. Egyptian regions participated in these exchanges in distinctive ways. Hence, control over wealth flows, access to coveted goods, contacts with privileged trading partners and attracting royal support represented significant moves in their strategies. A constant tension between different political models (centralized, confederacies of cities and territories, regional kingdoms) reemerged through the millennia. This often led to the collapse of the central authority (as it happened around 2160 bc) and was inspired, at least in part, by the political im...