Colin L. Masters (Australia)
The University of Melbourne
The Florey Institute
Colin Masters has focused his career on research in Alzheimer's disease and other neurodegenerative diseases, including Creutzfeldt-Jakob disease. His work over the last 40 years is widely acknowledged as having had a major influence on Alzheimer’s disease research world-wide, particularly the collaborative studies conducted with Konrad Beyreuther in which they discovered the proteolytic neuronal origin of the Aβ amyloid protein which causes Alzheimer’s disease. This work has led to the continued development of diagnostics and therapeutic strategies. More recently, his focus has been on describing the natural history of Alzheimer’s disease as a necessary preparatory step for disease modifying therapies. Professor Masters is a Professor of Dementia Research at the Florey Institute, and the University of Melbourne and a consultant at the Royal Melbourne Hospital. His achievements have been recognised by the receipt of many international awards.

Moderator of 1 Session

 Conference Calendar
SYMPOSIUM

ABETA TARGETING THERAPIES IN AD 2

Session Type
SYMPOSIUM
Date
Fri, 18.03.2022
Session Time
05:15 PM - 07:15 PM
Room
ONSITE PLENARY: 115-117
Chair(s)

Presenter of 1 Presentation

 Conference Calendar

PLASMA P-TAU181/AΒ42 RATIO PREDICTS AΒ-AMYLOID PET STATUS AND CORRELATES WITH CSF-P-TAU181/AΒ42 AND RATES OF FUTURE COGNITIVE DECLINE IN ALZHEIMER’S DISEASE.

Session Name
1540 - AD, LBD DIAGNOSIS, IMAGING & CLINICAL TRIALS (ID 79)
Session Type
SYMPOSIUM
Date
Sat, 19.03.2022
Session Time
09:10 AM - 11:10 AM
Room
ONSITE: 113
Lecture Time
09:10 AM - 09:25 AM
Presenter

Abstract

Aims

The ratio of phosphorylated tau (p-tau) over Aβ42-amyloid in CSF demonstrate superior performance over single biomarkers for predicting Aβ-PET status using automated immunoassay platforms. Recent studies show clearly that plasma Aβ42, and p-tau, can also predict Aβ-PET status, although only one study has explored the utility of the plasma p-tau181/Aβ42 ratio in predicting Aβ-PET burden. The current study investigated the ability of plasma p-tau181, Aβ40 and Aβ42 to predict amyloid-PET status.

Methods

This study used p-tau181, p-tau231, Aβ42, and Aβ40 levels using prototype Simoa assays to measure plasma samples from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study. PET, clinical, and demographic variables were also drawn from the AIBL study.

Results

The p-tau181/Aβ42 ratio showed the best prediction of Aβ-PET in all participants (AUC =0.905, 95%CI: 0.86-0.95) and in cognitively unimpaired (AUC=0.873; 0.80–0.94), and cognitively impaired (AUC=0.908; 0.82–1) adults. Plasma p-tau181 was associated moderately with CSF-p-tau181 (Elecsys®, Spearmans ρ=0.53, P<0.001). Use of the p-tau181/Aβ42 ratio improved this association significantly (Spearman’s ρ=0.74, P<0.0001). Plasma p-tau181 predicted abnormal CSF-Aβ levels with an AUC of 0.8 (0.73-0.88), which was also improved by use of the plasma p-tau181/Aβ42 ratio (AUC=0.816, 0.74-0.89). The p-tau181/Aβ42 ratio also predicted future rates of decline of cognition using the AIBL PACC and CDR-SoB (P<0.0001).

Conclusions

This high performing plasma p-tau181/Aβ42 ratio has excellent potential for development as both a screening and prognostic assay for preclinical Alzheimer’s disease (AD). Its utility for specific diagnosis in prodromal and clinical AD remains to be determined.

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