Results: 3

1.
FIGURE 3

FIGURE 3. Baseline CSF Measures of VILIP-1 (A), VILIP-1/Aβ42 (B), tau (C), tau/Aβ42 (D), p-tau181 (E), and p-tau181/Aβ42 (F) as Predictors of Conversion from CDR 0 to CDR 0.5 or Greater. From: VISININ-LIKE PROTEIN-1: DIAGNOSTIC AND PROGNOSTIC BIOMARKER IN ALZHEIMER DISEASE.

Kaplan-Meier estimates of the rates of conversion from CDR 0 to CDR 0.5 or greater as a function of CSF biomarker measures (dichotomized at the 85th percentile value) are shown. Analyses were adjusted for age, gender, education, and APOE ε4+ genotype. Cutoff values were 535 pg/ml, 440 pg/ml, 78 pg/ml, 1.13, 0.94, and 0.15 for VILIP-1, tau, p-tau181, VILIP-1/Aβ42, tau/Aβ42, and p-tau181/Aβ42, respectively. Adjusted hazard ratios were 3.74 (95% CI: 1.98–9.57, p=0.0023) for VILIP-1, 2.57 (95% CI: 1.31–6.97, p=0.0306) for tau, 1.72 (95% CI: 0.97–5.38, p=0.06) for p-tau181, 13.00 (95% CI: 4.38–30.90, p<0.0001) for VILIP-1/Aβ42, 9.82 (95% CI: 3.11–21.28, p<0.0001) for tau/Aβ42, and 7.83 (95% CI: 2.65–16.34, p<0.0001) for p-tau181/Aβ42.

Rawan Tarawneh, et al. Ann Neurol. ;70(2):274-285.
2.
FIGURE 1

FIGURE 1. Cerebrospinal Fluid (CSF) VILIP-1, tau, Aβ42, tau/Aβ42, and VILIP-1/Aβ42 levels by CDR Category in CNC, AD, and non-AD dementias. From: VISININ-LIKE PROTEIN-1: DIAGNOSTIC AND PROGNOSTIC BIOMARKER IN ALZHEIMER DISEASE.

(A) Mean (± SE) CSF VILIP-1 levels were significantly higher in CDR 0.5 (506 ± 20 pg/ml, n=72) and CDR ≥1 (558 ± 34 pg/ml, n=26) compared to CDR 0 (396 ± 10 pg/ml, n=211) and non-AD dementias (323 ± 40 pg/ml, n=19) (p<0.0001). (B) Mean (± SE) CSF VILIP-1 levels were significantly higher in CDR 0.5 and CDR ≥1 compared to PIB-negative CDR 0 (383 ± 14 pg/ml, n=95) and non-AD dementias (p<0.0001). (C–E) Mean CSF tau and tau/Aβ42 levels were significantly higher while mean CSF Aβ42 levels were significantly lower in CDR 0.5 and CDR ≥1 compared to CDR 0 (p<0.0001). (F) Mean (± SE) CSF VILIP-1/Aβ42 levels were significantly higher in CDR 0.5 (1.46 ± 0.08, n=69) and CDR ≥1 (1.79 ± 0.14, n=26) compared to CDR 0 (0.74 ± 0.03, n=200) and non-AD dementias (0.44 ± 0.03, n=19) (p<0.0001). One-Way ANOVA with Welch’s correction for unequal variances, Tukey post-hoc test was used for all group comparisons. (Similar results were obtained when Bonferroni’s correction was used for all group comparisons). Abbreviations: CNC, cognitively normal controls; AD, Alzheimer’s disease; SE, standard error.

Rawan Tarawneh, et al. Ann Neurol. ;70(2):274-285.
3.
FIGURE 2

FIGURE 2. From: VISININ-LIKE PROTEIN-1: DIAGNOSTIC AND PROGNOSTIC BIOMARKER IN ALZHEIMER DISEASE.

(A) Receiver Operator Curves (ROC) for the Diagnostic Utility of CSF Biomarkers and Ratios in Differentiating AD from CNC by Clinical Diagnosis. The area under the curve (AUC) ± standard error (SE) was 0.85 ± 0.02 for tau, 0.79 ± 0.03 for p-tau181, 0.79 ± 0.03 for Aβ42, 0.75 ± 0.03 for VILIP-1, 0.87 ± 0.02 for VILIP-1/Aβ42, 0.87 ± 0.02 for p-tau181/Aβ42, and 0.90 ± 0.02 for tau/Aβ42 (AD n=98, CNC n=211).
(B) Receiver Operator Curves (ROC) for the Diagnostic Utility of CSF Biomarkers and Ratios in Differentiating PIB-positive from PIB-negative Individuals. Study participants who underwent PET-PIB (n=156) were categorized by PIB status as PIB-positive (MCBP>0.18) (n=54) or PIB-negative (n=102) irrespective of clinical diagnoses. The area under the curve (AUC) ± standard error (SE) was 0.86 ± 0.03 for tau, 0.81 ± 0.04 for p-tau181, 0.87 ± 0.03 for Aβ42, 0.77 ± 0.04 for VILIP-1, 0.93 ± 0.02 for VILIP-1/Aβ42, 0.95 ± 0.02 for p-tau181/Aβ42, and 0.95 ± 0.02 for tau/Aβ42.
(C–D) Correlations of CSF VILIP-1 with nWBV and Hippocampal Volumes in AD. CSF VILIP-1 negatively correlated with (C) nWBV (unadjusted r= −0.448, p=0.003; adjusted r= −0.422, p=0.010), and (D) hippocampal volumes (unadjusted r= −0.483, p=0.001; adjusted r= −0.611, p=0.0001) in AD (n=43). Unadjusted linear regression lines are shown. Adjusted correlations included age, gender, and scanner type as co-variates. (E) Correlations Between CSF VILIP-1/Aβ42 and Amyloid Load by PET-PIB. CSF VILIP-1/Aβ42 (r=0.71, p<0.0001) correlated with PET-PIB mean cortical binding potential (MCBP) in the combined cohort (n=148). CSF VILIP-1/Aβ42 correlated with MCBP in AD (r=0.57, p=0.005) and CNC (r=0.67, p<0.0001) when examined separately. Individuals with AD (n=22) are represented by blue dots.

Rawan Tarawneh, et al. Ann Neurol. ;70(2):274-285.

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