Plasma p-tau217 emerges as top blood biomarker for Alzheimer’s amyloid triage
The review evaluates blood-based biomarkers for Alzheimer’s disease as anti-amyloid therapies expand. Investigators report that plasma p-tau217 consistently demonstrates the highest diagnostic accuracy for cortical amyloid pathology, and the p-tau217/Aβ1-42 ratio has secured FDA clearance for clinical triage. Complementary plasma assays, including Aβ42/40, GFAP, and neurofilament light chain, offer additional metrics for amyloid burden and neurodegeneration. The authors conclude that laboratory integration requires assay harmonization, standardized thresholds, and prospective validation to enable scalable, biomarker-guided dementia care.
The original study
Blood-based biomarkers in the anti-amyloid era of Alzheimer's disease: clinical utility, implementation challenges, and future directions.
- Authors
- Ho BL, Yang YH
- Journal
- Neurodegenerative disease management
- Type
- Journal Article, Review
- PMID
- 42800042
Original abstract
BACKGROUND: Implementation of disease-modifying anti-amyloid therapies for Alzheimer's disease remains constrained by the cost and procedural burden of positron emission tomography and cerebrospinal fluid testing. This review evaluates blood-based biomarkers in therapeutic pathways. METHODS: PubMed/MEDLINE and Embase were searched for literature published from January 2018 onward, with earlier landmark studies included when relevant. Evidence was synthesized on plasma biomarkers in treatment eligibility, biological staging, longitudinal monitoring, therapeutic response, and risk stratification for amyloid-related imaging abnormalities. RESULTS: Among assays, plasma p-tau217 consistently demonstrates the highest diagnostic accuracy for detecting cortical amyloid pathology across clinical settings. The plasma p-tau217/Aβ1-42 ratio is the first blood-based assay cleared by the FDA to identify amyloid pathology, supporting clinical triage. Complementary biomarkers, including plasma Aβ42/40, glial fibrillary acidic protein, and neurofilament light chain, reflect amyloid burden, astroglial activation, and neurodegeneration. Clinical adoption remains limited by inter-assay variability, inconsistent diagnostic thresholds, and the lack of surrogate endpoints for treatment monitoring and adverse-event assessment. CONCLUSIONS: Blood-based biomarkers are best incorporated into structured, stepwise diagnostic and therapeutic frameworks rather than replacing established reference standards. Progress will require assay harmonization, prospective validation, and interpretable biomarker-guided care pathways to support scalable, safe implementation of disease-modifying therapies in routine dementia care.