Blood plasma phosphorylated-tau isoforms track CNS change in Alzheimer’s disease

Author:

Barthélemy Nicolas R.1ORCID,Horie Kanta1ORCID,Sato Chihiro1ORCID,Bateman Randall J.123ORCID

Affiliation:

1. Department of Neurology, Washington University School of Medicine, St. Louis, MO

2. Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO

3. Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine, St. Louis, MO

Abstract

Highly sensitive and specific plasma biomarkers for Alzheimer’s disease (AD) have the potential to improve diagnostic accuracy in the clinic and facilitate research studies including enrollment in prevention and treatment trials. We recently reported CSF tau hyperphosphorylation, especially on T217, is an accurate predictor of β-amyloidosis at asymptomatic and symptomatic stages. In the current study, we determine by mass spectrometry the potential utility of plasma p-tau isoforms to detect AD pathology and investigate CSF and plasma tau isoforms’ profile relationships. Plasma tau was truncated as previously described in CSF. CSF and plasma measures of p-tau-217 and p-tau-181 were correlated. No correlation was found between CSF and plasma on total-tau levels and pS202 measures. We found p-tau-217 and p-tau-181 were highly specific for amyloid plaque pathology in the discovery cohort (n = 36, AUROC = 0.99 and 0.98 respectively). In the validation cohort (n = 92), p-tau-217 measures were still specific to amyloid status (AUROC = 0.92), and p-tau-181 measures were less specific (AUROC = 0.75).

Funder

Alzheimer’s Association

Rainwater Charitable Foundation

National Institutes of Health

National Institute of Neurological Disorders and Stroke

Tau SILK Consortium

AbbVie

Biogen

Eli Lilly and Company

Coins for Alzheimer’s Research Trust

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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