Scatterplot showing log-transformed total-tau/Aβ₄₂ ratio and power-transformed SPARE-AD (A) and power transformed SPARE-AD and ADAS-Cog score (B).

<p>The marginal box plots on x-axis represent the distribution of the power transformed SPARE-AD and the marginal box-plots on the y-axis represent the t-tau/Aβ₄₂ ratio (A) and ADAS-Cog (B) values.</p

Regression of MIP-1α without (A), with adjustment for age (B) and with adjustment for age and clinical diagnosis (C), against grey matter (GM) volumes.

<p>The color scale represents in blue a decrease in GM volumes associated to increased levels of the biomarker in plasma. White matter changes (in red) indicate abnormal periventricular brain tissue, commonly associated with leukoaraiosis.</p

Characteristics of subjects included in the study.

<p>Characteristics of subjects included in the study.</p

Evaluated immunoassay kits, including assay characteristics and CSF dilutions.

<p>Evaluated immunoassay kits, including assay characteristics and CSF dilutions.</p

Unstandardized coefficients derived from multiple regression models studying the association between RBM plasma analytes and SPARE AD adjusted for clinical category, APOE ε4 presence, age and CSF signature.

<p>Unstandardized coefficients derived from multiple regression models studying the association between RBM plasma analytes and SPARE AD adjusted for clinical category, APOE ε4 presence, age and CSF signature.</p

Unstandardized coefficients derived from multiple regression models studying the association between RBM plasma analytes and SPARE AD adjusted for clinical diagnosis, age, and APOE ε4 presence.

<p>Unstandardized coefficients derived from multiple regression models studying the association between RBM plasma analytes and SPARE AD adjusted for clinical diagnosis, age, and APOE ε4 presence.</p

Baseline demographic and clinical characteristics of study participants.

<p>Baseline demographic and clinical characteristics of study participants.</p

Short-term biotemporal stability of measurable and technically precise analytes in CSF.

<p>Biotemporal variation between paired samples over an 8-week interval for (a) core AD biomarkers, (b) Aβ and tau-independent markers of neurodegeneration, (c) metabolic and oxidative stress markers, (d) markers of inflammation and inflammatory modulators, and (e) vascular injury markers. Samples plotted for each analyte, with baseline concentrations connected to corresponding paired week 8 concentrations. Plotted using a log scale, all units converted to pg/mL. <i>N</i> = 9 pairs for each analyte, concentrations averaged across three technical replicates. Each analyte plot is labeled with the median biotemporal CV (%). A CV < 15% indicated low intra-individual variation.</p

Regression of cortisol without adjustment (A), with adjustment for age (B) and with adjustment for age and clinical diagnosis (C), against regional grey matter (GM) volumes.

<p>The color scale represents in blue a decrease in GM volumes associated to a increase levels of the biomarker in plasma. White matter changes (in red) indicate abnormal brain tissue, commonly associated with leukoaraiosis.</p

Structure of the assay stability evaluation scheme.

<p>Duplicate samples were located on individual plates as shown, to allow for assessment of intra- and inter-assay precision and biotemporal stability of analyte measures. T1 and T2 denote repeat-collected CSFs from the same individual; A-C indicate different aliquots of the same CSF sample. <i>N</i> = 35 samples were included on each individual plate, in addition to a standard curve and spiked controls.</p