The approval of anti-amyloid therapies has reshaped Alzheimer’s disease from a clinically defined syndrome to a biologically confirmed and treatment-oriented condition. This transition places biomarkers, particularly amyloid positron emission tomography (Aβ-PET), at the centre of diagnostic precision, patient selection, safety governance, and therapeutic monitoring. Aβ-PET provides high specificity for confirming cerebral amyloid pathology, especially in cases with discordant or inconclusive fluid biomarkers, and supports staging through semi-quantitative assessment using standardised Centiloid metrics. In patients considered for anti-amyloid therapies, baseline Aβ-PET refines eligibility and risk–benefit profiling when integrated with MRI and APOE genotyping. During treatment, longitudinal Aβ-PET enables objective assessment of pharmacodynamic target engagement and treatment-related amyloid clearance, supporting response-adapted strategies and, in selected cases, therapy discontinuation. Beyond its clinical role, Aβ-PET has strategic organisational and economic implications. Its value is maximised when embedded within structured, stepwise diagnostic pathways that use scalable fluid biomarkers for triage and reserve Aβ-PET for high-impact decisions. However, implementation is challenged by regional heterogeneity, capacity constraints, and limited harmonisation across centres. Coordinated hub-and-spoke models, quantitative standardisation, and prospective registry-based data collection are essential to ensure the equitable and sustainable integration of anti-amyloid therapies into clinical practice. Aβ-PET has evolved from a confirmatory diagnostic tool to a strategic instrument that enables biologically driven, outcome-oriented care for patients with Alzheimer’s disease.
Precision pathways: optimising amyloid PET for sustainable Alzheimer’s disease care
Cagnin A.;Cecchin D.;
2026
Abstract
The approval of anti-amyloid therapies has reshaped Alzheimer’s disease from a clinically defined syndrome to a biologically confirmed and treatment-oriented condition. This transition places biomarkers, particularly amyloid positron emission tomography (Aβ-PET), at the centre of diagnostic precision, patient selection, safety governance, and therapeutic monitoring. Aβ-PET provides high specificity for confirming cerebral amyloid pathology, especially in cases with discordant or inconclusive fluid biomarkers, and supports staging through semi-quantitative assessment using standardised Centiloid metrics. In patients considered for anti-amyloid therapies, baseline Aβ-PET refines eligibility and risk–benefit profiling when integrated with MRI and APOE genotyping. During treatment, longitudinal Aβ-PET enables objective assessment of pharmacodynamic target engagement and treatment-related amyloid clearance, supporting response-adapted strategies and, in selected cases, therapy discontinuation. Beyond its clinical role, Aβ-PET has strategic organisational and economic implications. Its value is maximised when embedded within structured, stepwise diagnostic pathways that use scalable fluid biomarkers for triage and reserve Aβ-PET for high-impact decisions. However, implementation is challenged by regional heterogeneity, capacity constraints, and limited harmonisation across centres. Coordinated hub-and-spoke models, quantitative standardisation, and prospective registry-based data collection are essential to ensure the equitable and sustainable integration of anti-amyloid therapies into clinical practice. Aβ-PET has evolved from a confirmatory diagnostic tool to a strategic instrument that enables biologically driven, outcome-oriented care for patients with Alzheimer’s disease.
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