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Predictive performance for Aβ-PET positivity Predictive performance of p-tau markers is shown in panel A, and Aβ, GFAP, and NFL in panel B. Biomarkers were examined as continuous variables. Unadjusted logistic regression; discrimination quantified by AUCs (95% CI). PiB-PET scan and visual read of Aβ positivity were available for 46 participants at <t>baseline.</t> <t>P-tau217</t> was measured with both Lumipulse assay and NULISAseq™ CNS Disease Panel 120, all other markers were measured with NULISAseq™ CNS Disease Panel 120. Aβ=beta-amyloid; AUC=area under the curve; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; PiB-PET=Pittsburgh compound B positron emission tomography; p-tau=phosphorylated tau.
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Predictive performance for Aβ-PET positivity Predictive performance of p-tau markers is shown in panel A, and Aβ, GFAP, and NFL in panel B. Biomarkers were examined as continuous variables. Unadjusted logistic regression; discrimination quantified by AUCs (95% CI). PiB-PET scan and visual read of Aβ positivity were available for 46 participants at <t>baseline.</t> <t>P-tau217</t> was measured with both Lumipulse assay and NULISAseq™ CNS Disease Panel 120, all other markers were measured with NULISAseq™ CNS Disease Panel 120. Aβ=beta-amyloid; AUC=area under the curve; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; PiB-PET=Pittsburgh compound B positron emission tomography; p-tau=phosphorylated tau.
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Predictive performance for Aβ-PET positivity Predictive performance of p-tau markers is shown in panel A, and Aβ, GFAP, and NFL in panel B. Biomarkers were examined as continuous variables. Unadjusted logistic regression; discrimination quantified by AUCs (95% CI). PiB-PET scan and visual read of Aβ positivity were available for 46 participants at <t>baseline.</t> <t>P-tau217</t> was measured with both Lumipulse assay and NULISAseq™ CNS Disease Panel 120, all other markers were measured with NULISAseq™ CNS Disease Panel 120. Aβ=beta-amyloid; AUC=area under the curve; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; PiB-PET=Pittsburgh compound B positron emission tomography; p-tau=phosphorylated tau.
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Predictive performance for Aβ-PET positivity Predictive performance of p-tau markers is shown in panel A, and Aβ, GFAP, and NFL in panel B. Biomarkers were examined as continuous variables. Unadjusted logistic regression; discrimination quantified by AUCs (95% CI). PiB-PET scan and visual read of Aβ positivity were available for 46 participants at <t>baseline.</t> <t>P-tau217</t> was measured with both Lumipulse assay and NULISAseq™ CNS Disease Panel 120, all other markers were measured with NULISAseq™ CNS Disease Panel 120. Aβ=beta-amyloid; AUC=area under the curve; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; PiB-PET=Pittsburgh compound B positron emission tomography; p-tau=phosphorylated tau.
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Image Search Results


Predictive performance for Aβ-PET positivity Predictive performance of p-tau markers is shown in panel A, and Aβ, GFAP, and NFL in panel B. Biomarkers were examined as continuous variables. Unadjusted logistic regression; discrimination quantified by AUCs (95% CI). PiB-PET scan and visual read of Aβ positivity were available for 46 participants at baseline. P-tau217 was measured with both Lumipulse assay and NULISAseq™ CNS Disease Panel 120, all other markers were measured with NULISAseq™ CNS Disease Panel 120. Aβ=beta-amyloid; AUC=area under the curve; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; PiB-PET=Pittsburgh compound B positron emission tomography; p-tau=phosphorylated tau.

Journal: medRxiv

Article Title: Blood Biomarkers of Alzheimer’s Disease Neuropathology, Cognition, and Response to a Multidomain Lifestyle Intervention: Secondary analysis of the FINGER Randomized Controlled Dementia Risk Reduction Trial

doi: 10.64898/2026.10.02.26364486

Figure Lengend Snippet: Predictive performance for Aβ-PET positivity Predictive performance of p-tau markers is shown in panel A, and Aβ, GFAP, and NFL in panel B. Biomarkers were examined as continuous variables. Unadjusted logistic regression; discrimination quantified by AUCs (95% CI). PiB-PET scan and visual read of Aβ positivity were available for 46 participants at baseline. P-tau217 was measured with both Lumipulse assay and NULISAseq™ CNS Disease Panel 120, all other markers were measured with NULISAseq™ CNS Disease Panel 120. Aβ=beta-amyloid; AUC=area under the curve; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; PiB-PET=Pittsburgh compound B positron emission tomography; p-tau=phosphorylated tau.

Article Snippet: The n (%) of Aβ-PET positives among those with normal, intermediate, and pathological plasma p-tau217 (Lumipulse) was 11/36 (31%), 4/6 (67%), and 4/4 (100%), respectively.

Techniques: Positron Emission Tomography

Associations between baseline biomarker levels and cognition (NTB Global cognition, primary trial outcome) Estimates (95% CI) were obtained from linear regression models (for baseline cognition, A) and mixed-effects models (for cognitive change, B), using marginal prediction methods to derive interpretable effect estimates. Results are interpreted as differences in baseline cognitive performance (A) or cognitive change in two years (B), per 1 standard deviation (SD) higher baseline biomarker level, in the whole cohort (irrespective of randomization). Negative estimates indicate worse cognitive performance or less favorable cognitive trajectory (less improvement) with increasing baseline biomarker levels. Analyses were adjusted for baseline age, sex, education, study site, APOE genotype, body mass index (BMI), and estimated glomerular filtration rate (eGFR) as an indicator of renal function. Baseline analysis n=1220 (Lumipulse p-tau217) and n=1223 (other biomarkers); longitudinal analysis n=1154 (Lumipulse p-tau217) and n=1157 (other biomarkers). Aβ=beta-amyloid; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; NTB=neuropsychological test battery; p-tau=phosphorylated tau.

Journal: medRxiv

Article Title: Blood Biomarkers of Alzheimer’s Disease Neuropathology, Cognition, and Response to a Multidomain Lifestyle Intervention: Secondary analysis of the FINGER Randomized Controlled Dementia Risk Reduction Trial

doi: 10.64898/2026.10.02.26364486

Figure Lengend Snippet: Associations between baseline biomarker levels and cognition (NTB Global cognition, primary trial outcome) Estimates (95% CI) were obtained from linear regression models (for baseline cognition, A) and mixed-effects models (for cognitive change, B), using marginal prediction methods to derive interpretable effect estimates. Results are interpreted as differences in baseline cognitive performance (A) or cognitive change in two years (B), per 1 standard deviation (SD) higher baseline biomarker level, in the whole cohort (irrespective of randomization). Negative estimates indicate worse cognitive performance or less favorable cognitive trajectory (less improvement) with increasing baseline biomarker levels. Analyses were adjusted for baseline age, sex, education, study site, APOE genotype, body mass index (BMI), and estimated glomerular filtration rate (eGFR) as an indicator of renal function. Baseline analysis n=1220 (Lumipulse p-tau217) and n=1223 (other biomarkers); longitudinal analysis n=1154 (Lumipulse p-tau217) and n=1157 (other biomarkers). Aβ=beta-amyloid; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; NTB=neuropsychological test battery; p-tau=phosphorylated tau.

Article Snippet: The n (%) of Aβ-PET positives among those with normal, intermediate, and pathological plasma p-tau217 (Lumipulse) was 11/36 (31%), 4/6 (67%), and 4/4 (100%), respectively.

Techniques: Biomarker Discovery, Standard Deviation, Filtration, Analysis, Battery

Intervention effect modification by baseline biomarker levels (outcome NTB Global cognition, primary trial outcome) Estimates (95% CI) were obtained from linear mixed-effects models, using marginal prediction methods to derive interpretable effect estimates. Estimates are interpreted as difference between the intervention and control groups in cognitive change per year; positive estimates indicate more favorable cognitive change in the intervention group. Biomarker × group × time interactions were examined to assess whether baseline biomarker levels modified the intervention effects on cognition, i.e., whether the differences in cognitive change between intervention and control groups differed by baseline biomarker levels. Interactions with p>0.05 indicate that the intervention effect did not significantly differ by baseline biomarker levels. Interactions were derived from models where biomarkers were entered as continuous variables, but for visualization, estimates for intervention effect are presented within biomarker strata (below median = blue diamond, above median = red circle). Analyses were adjusted for age, sex, education, study site, APOE genotype, body mass index (BMI), and estimated glomerular filtration rate (eGFR). Aβ=beta-amyloid; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; NTB=neuropsychological test battery; p-tau=phosphorylated tau.

Journal: medRxiv

Article Title: Blood Biomarkers of Alzheimer’s Disease Neuropathology, Cognition, and Response to a Multidomain Lifestyle Intervention: Secondary analysis of the FINGER Randomized Controlled Dementia Risk Reduction Trial

doi: 10.64898/2026.10.02.26364486

Figure Lengend Snippet: Intervention effect modification by baseline biomarker levels (outcome NTB Global cognition, primary trial outcome) Estimates (95% CI) were obtained from linear mixed-effects models, using marginal prediction methods to derive interpretable effect estimates. Estimates are interpreted as difference between the intervention and control groups in cognitive change per year; positive estimates indicate more favorable cognitive change in the intervention group. Biomarker × group × time interactions were examined to assess whether baseline biomarker levels modified the intervention effects on cognition, i.e., whether the differences in cognitive change between intervention and control groups differed by baseline biomarker levels. Interactions with p>0.05 indicate that the intervention effect did not significantly differ by baseline biomarker levels. Interactions were derived from models where biomarkers were entered as continuous variables, but for visualization, estimates for intervention effect are presented within biomarker strata (below median = blue diamond, above median = red circle). Analyses were adjusted for age, sex, education, study site, APOE genotype, body mass index (BMI), and estimated glomerular filtration rate (eGFR). Aβ=beta-amyloid; GFAP=glial fibrillary acidic protein; NFL=neurofilament light chain; NTB=neuropsychological test battery; p-tau=phosphorylated tau.

Article Snippet: The n (%) of Aβ-PET positives among those with normal, intermediate, and pathological plasma p-tau217 (Lumipulse) was 11/36 (31%), 4/6 (67%), and 4/4 (100%), respectively.

Techniques: Modification, Biomarker Discovery, Control, Derivative Assay, Filtration, Battery