CSF Aβ40 and P-Tau181 Might Differentiate Atypical from Typical AD Phenotypes: Preliminary Evidence

Neurodegenerative Diseases

Verde F.a,b· Aiello E.N.a,c· Giacopuzzi Grigoli E.a,d· Milone I.a· Dubini A.e· Ratti A.a,f· Poletti B.a· Ticozzi N.a,b· Silani V.a,b

Author affiliations

aIRCCS Istituto Auxologico Italiano, Department of Neurology and Laboratory of Neuroscience, Milan, Italy
bDepartment of Pathophysiology and Transplantation, “Dino Ferrari Center”, Università degli Studi di Milano, Milan, Italy
cPhD Program in Neuroscience, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy
dNeurology Residency Program, Università degli Studi di Milano, Milan, Italy
eIRCCS Istituto Auxologico Italiano, Department of Laboratory Medicine, Laboratory of Clinical Chemistry, Milan, Italy
fDepartment of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy

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Article / Publication Details

First-Page Preview

Abstract of Brief Report

Received: July 21, 2022
Accepted: August 18, 2022
Published online: September 15, 2022

Number of Print Pages: 4
Number of Figures: 0
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: https://www.karger.com/NDD

Abstract

Objectives: This study aimed at testing whether CSF levels of amyloid β42 (Aβ42), Aβ40, total tau, and phosphorylated tau (P-tau181) individually contribute to the identification of atypical phenotypes among a retrospective cohort of probable Alzheimer’s disease (AD) patients diagnosed by means of the ratio between Aβ42 and Aβ40 (Aβ42/40). Methods: The retrospective study cohort comprised 50 probable AD patients diagnosed by means of the ratio between Aβ42 and Aβ40 (Aβ42/40) and for whom total tau and P-tau181 values were also available. Patients were clinically classified as typical, amnestic-predominant AD (N = 39; 16 males; mean age: 73.4 ± 7.6 years; mean disease duration: 27.4 ± 24.7 months), or atypical phenotypes (N = 11; 6 males; mean age: 70.2 ± 6.5 years; mean disease duration: 35.5 ± 24.9 months) – i.e., posterior cortical atrophy (N = 4), logopenic-variant primary progressive aphasia (N = 4), and behavioural variant AD (N = 3). A logistic regression allowed predicting the occurrence of atypical versus typical phenotypes based on age, sex, and Aβ42, Aβ40, total tau, and P-tau181 levels. Results: Atypical and typical AD patients were comparable for Aβ42/40 values. Only Aβ40 and P-tau181 levels positively (p = 0.015) and negatively (p = 0.019) predicted the occurrence of atypical AD phenotypes, respectively. Classification precision was of 86%, yielding excellent specificity (94.9%) but poor sensitivity (54.5%). Conclusions: The present study delivers promising, albeit preliminary, evidence on the utility of Aβ40 and P-tau181 CSF biomarkers in differentiating atypical from typical Aβ42/40-confirmed AD phenotypes, prompting further research and confirmation on larger cohorts.

© 2022 S. Karger AG, Basel

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First-Page Preview

Abstract of Brief Report

Received: July 21, 2022
Accepted: August 18, 2022
Published online: September 15, 2022

Number of Print Pages: 4
Number of Figures: 0
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: https://www.karger.com/NDD

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