Longitudinal change of CSF tau and Aβ42.

<p>The figure shows the mean baseline and follow-up levels of CSF tau (panel A) and CSF Aβ42 (panel B) in healthy controls (HC), that were followed for 4 years (y), and in two cohorts of patients with Alzheimer's disease (AD) that were followed for one or two years, respectively. Error bars represent standard errors of the mean. The figure illustrates that differences between controls and AD patients by far surpass the within-group differences over time.</p

Demographic characteristics of the AD patients and the age-matched controls at baseline and follow-up.

<p>Values are means±SD, except as noted otherwise.</p>a<p>p<0.001 vs Controls.</p><p>Abbreviations: 1-year AD cohort, AD patients with approximately one year between baseline and follow-up lumbar puncture; 2-year AD cohort, AD patients with approximately two years between baseline and follow-up lumbar puncture; Controls, healthy controls followed for 4 years; APOE ε4 carrier, at least one apolipoprotein E ε4 allele; MMSE, Mini-Mental State Examination.</p

Baseline and follow-up levels of CSF tau and Aβ42 in the AD patients and age-matched controls.

<p>Values are means±SD except if noted otherwise.</p>a<p>p<0.001 vs Controls.</p>b<p>p<0.05 vs baseline.</p><p>Abbreviations: CSF, cerebrospinal fluid; 1-year AD cohort, subjects with Alzheimer's disease with an interval between baseline and follow-up lumbar puncture of approximately one year; 2-year AD cohort, subjects with Alzheimer's disease with an interval between baseline and follow-up lumbar puncture of approximately two years. Controls, healthy controls followed for 4 years.</p

Additional file 1: of Greater tau load and reduced cortical thickness in APOE ε4-negative Alzheimer’s disease: a cohort study

Supplementary material. (DOCX 286 kb

Sample characteristics of the study population.

<p>Sample characteristics of the study population.</p

Multivariate linear regression analyses of MD and FA in the dorsal and ventral cingulum, the SLF, and the CST in cognitively healthy elderly (<i>n</i> = 132) and prodromal AD subjects (<i>n</i> = 83) unadjusted (model 1) and adjusted (model 2) for WMH volume, respectively.

<p>Multivariate linear regression analyses of MD and FA in the dorsal and ventral cingulum, the SLF, and the CST in cognitively healthy elderly (<i>n</i> = 132) and prodromal AD subjects (<i>n</i> = 83) unadjusted (model 1) and adjusted (model 2) for WMH volume, respectively.</p

Effect size of group mean expressed as Cohen’s <i>d</i> and group size (<i>n</i>, patient group + control group) for WMH in the present study and various pathological conditions previously studied using DTI.

<p>Effect size of group mean expressed as Cohen’s <i>d</i> and group size (<i>n</i>, patient group + control group) for WMH in the present study and various pathological conditions previously studied using DTI.</p

Graphical rendering of tractographies in a representative subject.

<p>Tractographies of the left-hand side of the dorsal cingulum (A), the ventral cingulum (B), the superior longitudinal fasciculus (SLF; C), and the corticospinal tract (CST; D) segmented from a whole-brain tractography and superimposed on a mid-sagittal FA map.</p

FLAIR images of two different representative subjects with different WMH load.

<p>Subject A represents lower WMH load (i.e. a WMH volume ≤ 0.5% of the intracranial volume that corresponded approximately to Fazekas grade 0–1) and subject B higher WMH load (i.e. a WMH volume ≥ 1% of the intracranial volume that corresponded approximately to Fazekas grade 2–3), with arrows indicating example regions with WMH.</p

Additional file 1 of Plasma N-terminal containing tau fragments (NTA-tau): a biomarker of tau deposition in Alzheimer’s Disease

Additional file 1: Supplementary Figure 1. Plasma NTA-tau levels across AA criteria for staging AD using PET (BioFINDER-2). Supplementary Figure 2. Regional associations between plasma NTA-tau, p-tau181, NfL and GFAP levels with Aβ-PET, tau-PET and cortical thickness (BioFINDER-2). Supplementary Table 1. Characteristics of the subsample with available plasma t-tau (BioFINDER-2). Supplementary Table 2. Plasma NTA-tau levels by diagnosis (BioFINDER-2). Supplementary Table 3. Characteristics of the sample by AT status (BioFINDER-2). Supplementary Table 4. Plasma NTA-tau levels by AT status (BioFINDER-2). Supplementary Table 5. Characteristics of the sample by Braak stages (BioFINDER-2). Supplementary Table 6. Plasma NTA-tau levels by Braak stages (BioFINDER-2). Supplementary Table 7. Plasma NTA-tau levels by AA criteria for staging AD (BioFINDER-2). Supplementary Table 8. Plasma NTA-tau levels by diagnosis (BioFINDER-1). Supplementary Table 9. Comparison between models including/excluding an interaction between plasma NTA-tau and Aβ-status (BioFINDER-2 and -1). Supplementary Table 10. Proportion of variation of plasma biomarker levels explained by amyloid and tau (BioFINDER-2). Supplementary Table 11. Characteristics of the longitudinal tau-PET sample (BioFINDER-2). Supplementary Table 12. Characteristics of the longitudinal MRI sample (BioFINDER-2). Supplementary Table 13. Characteristics of the longitudinal MRI sample (BioFINDER-1). Supplementary Table 14. Characteristics of the longitudinal cognition sample (BioFINDER-2). Supplementary Table 15. Characteristics of the longitudinal cognition sample (BioFINDER-1). Supplementary Table 16. Characteristics of the longitudinal plasma NTA-tau (BioFINDER-1)