PrecivityAD2 detects the molecular signature of amyloid pathology by measuring several proteins in a blood sample. Alzheimer’s disease is characterized by the accumulation of amyloid plaques and abnormal tau proteins in the brain, biological changes that can begin years before dementia becomes apparent. The test quantifies the ratio of two amyloid-beta molecules, Aβ42 and Aβ40, together with two tau-related biomarkers, phosphorylated tau217 and total tau217. The relative abundance of these molecules provides information about whether amyloid pathology is likely to be present. In particular, a reduced Aβ42-to-Aβ40 ratio is associated with amyloid deposition, while elevations in phosphorylated and total tau can reflect downstream changes linked to neurodegeneration. By combining these measurements, PrecivityAD2 generates a composite result intended to support clinical evaluation.

Unlike many blood tests that rely on antibody-based immunoassays, PrecivityAD2 uses high-resolution mass spectrometry. This analytical approach separates molecules according to their mass and chemical properties, allowing researchers to distinguish closely related protein fragments and to measure them quantitatively. That distinction is especially important for amyloid-beta and tau, which exist in multiple molecular forms that may differ by only a small structural feature. Mass spectrometry can target these specific molecular species with high analytical precision, reducing the risk that similar proteins or fragments will be mistaken for the biomarkers of interest. The method also enables simultaneous examination of several Alzheimer’s-associated signals in a single blood draw, creating a biochemical profile rather than relying on one marker alone.

The availability of such a test could change how clinicians investigate memory loss and other cognitive symptoms. Current biological confirmation of Alzheimer’s pathology may involve cerebrospinal fluid collected through a lumbar puncture or positron emission tomography scans that use radioactive tracers to visualize amyloid in the brain. Both approaches can be highly informative, but they may be expensive, time-consuming, invasive or unavailable in many clinical settings. A blood test can be collected in an ordinary medical laboratory and may make biomarker assessment accessible to a substantially larger number of patients. However, the result is not intended to replace a complete neurological evaluation. Physicians must interpret it alongside a patient’s symptoms, medical history, cognitive testing, examination findings and, when necessary, imaging or cerebrospinal fluid data.

Studies reported by WashU and C2N have found that PrecivityAD2 can identify Alzheimer’s-related amyloid pathology with more than 90% accuracy in evaluated patient groups. The test has shown performance comparable to established cerebrospinal fluid measurements and amyloid brain scans, including among people with mild cognitive symptoms. Such results are important because early symptomatic patients often occupy a diagnostic gray zone: their memory or thinking problems may be subtle, yet the underlying disease process may already be advancing. A reliable blood biomarker could help separate patients who are likely to have amyloid pathology from those whose symptoms arise from another condition. At the same time, accuracy is not absolute, and a positive or negative result may require confirmation when it conflicts with the broader clinical picture.

The timing of the FDA clearance is particularly consequential because the first treatments capable of slowing the progression of Alzheimer’s disease have recently become available. These therapies are designed for patients with confirmed amyloid pathology and are generally more useful when introduced earlier in the course of disease, before extensive neuronal damage has occurred. A faster route to biological assessment could help eligible patients and their physicians consider treatment sooner, while also preventing people without amyloid pathology from receiving therapies that are unlikely to benefit them. Earlier information may additionally support planning for follow-up care, clinical trial participation and management of other medical conditions that can worsen cognitive performance. The test therefore has potential value not only as a diagnostic tool but also as part of a broader treatment decision-making process.

The scientific foundation for PrecivityAD2 emerged from research conducted in the laboratories of Bateman and Holtzman at WashU Medicine. Their work investigated how amyloid-beta and tau are produced, transported and cleared in the brain and cerebrospinal fluid. They helped pioneer stable isotope-linked kinetics, or SILK, a technique that uses labeled molecules to track the production and removal of proteins in living people. By measuring how quickly amyloid-beta is generated and cleared, researchers gained a more detailed view of the biological processes that precede plaque formation. This research provided a framework for developing sensitive assays capable of detecting disease-related changes in blood, where Alzheimer’s biomarkers are present at far lower concentrations than in cerebrospinal fluid.

Bateman, Holtzman and colleagues worked with WashU’s Office of Technology Management to patent components of the technology and co-founded C2N Diagnostics in 2007 to pursue commercial development. C2N obtained exclusive commercial licenses to relevant inventions from the university and refined the assays for clinical use. The company’s work illustrates how discoveries made in academic laboratories can move through intellectual property development, analytical validation and regulatory review before reaching physicians. C2N now employs more than 120 researchers, physicians and other professionals and is expanding its headquarters in St. Louis’ Cortex Innovation District. The continuing research relationship between WashU Medicine and C2N has helped advance the test from an experimental measurement of Alzheimer’s biology to a regulated product intended for use in healthcare systems.

FDA clearance means that the agency reviewed evidence supporting the test’s analytical and clinical performance and determined that it could be marketed for its specified use. It does not mean that PrecivityAD2 can diagnose every case of Alzheimer’s disease, detect all causes of cognitive decline or replace professional judgment. The result identifies the likelihood of amyloid plaques associated with Alzheimer’s pathology, while the patient’s symptoms and other findings remain essential to determining whether Alzheimer’s disease is the cause of impairment. Broader marketing may nevertheless encourage adoption by clinicians and health systems that require regulatory authorization before incorporating a diagnostic into practice. It may also help insurers evaluate coverage, potentially reducing financial barriers to testing. As blood biomarkers become more sophisticated, PrecivityAD2 could help establish a new diagnostic pathway in which Alzheimer’s biology is assessed earlier, more conveniently and at a scale that was previously difficult to achieve.

Subject of Research: Blood-based diagnosis and biomarker detection for Alzheimer’s disease.

Article Title: FDA Clears Blood Test Designed to Detect Alzheimer’s-Linked Amyloid Pathology

Web References: https://medicine.washu.edu/news/alzheimers-blood-test-performs-as-well-as-fda-approved-spinal-fluid-tests/ ; https://neurology.wustl.edu/people/randall-bateman-md/ ; https://holtzmanlab.wustl.edu/people/david-m-holtzman-md/ ; https://medicine.washu.edu/

References: Washington University School of Medicine in St. Louis; C2N Diagnostics; U.S. Food and Drug Administration.

Image Credits: Matt Miller/WashU Medicine.

Keywords: Alzheimer’s disease, PrecivityAD2, blood test, amyloid beta, tau protein, p-tau217, mass spectrometry, biomarkers, neurology, dementia, early diagnosis, C2N Diagnostics, Washington University School of Medicine.

The focus of this comprehensive investigation was the accumulation of tau, a protein closely linked with Alzheimer’s disease progression. The study utilized state-of-the-art positron emission tomography (PET) imaging with a newly developed tau tracer to detect abnormal tau protein tangles in the brains of over 1,500 cognitively normal and mildly impaired older adults. Notably, this cohort was racially and ethnically diverse, encompassing Black, Hispanic, and non-Hispanic white participants, which allowed for a robust analysis of the influence of ethnoracial identity on Alzheimer’s biomarkers.

Results indicated that Black and Hispanic individuals exhibited significantly higher tau burden in key memory-associated regions of the medial temporal lobe compared to non-Hispanic white participants, even in the absence of overt amyloid plaque buildup, which is traditionally considered the hallmark initiating event in Alzheimer’s pathology. This dissociation between amyloid and tau pathology among different groups disrupts the conventionally understood sequence of biomarker development and suggests alternative disease trajectories may be operative in diverse populations.

Furthermore, the relationship between biological markers and cognitive performance revealed complex interactions. While elevated tau correlated with impaired memory across the cohort, the interplay between amyloid plaque levels and memory decline was only evident in non-Hispanic white and Hispanic groups. Remarkably, in Black participants, amyloid levels did not strengthen the association between tau pathology and memory deficits. This finding implies that other, perhaps non-neuropathological, factors might be more influential in cognitive deterioration within this population.

Experts propose that beyond amyloid and tau pathology, additional elements such as vascular health comorbidities, chronic stress exposure, social determinants of health, and other systemic conditions could be driving memory decline in Black adults. This multifactorial influence necessitates a multidisciplinary approach integrating neurobiology, epidemiology, and social sciences to address Alzheimer’s disease in a clinically meaningful way across all communities.

The research also identified potential technical limitations associated with the tau PET tracer used. The imaging agent occasionally produced signals emanating from adjacent brain regions, confounding the interpretation of tau accumulation patterns. This observation underscores the imperative for rigorous validation of neuroimaging tools in heterogeneous populations to ensure the biological accuracy and reliability of PET data, preventing misinterpretation that could misguide diagnostic or therapeutic decisions.

This study, emerging from the Health and Aging Brain Study–Health Disparities (HABS-HD), represents one of the most extensive neuroimaging efforts targeting Alzheimer’s-related brain changes in racially and ethnically diverse aging populations within the United States. The success of this endeavor owes much to the advanced imaging infrastructure at Stevens INI, which facilitated high-resolution PET imaging and comprehensive data analysis.

Principal investigators emphasize that these findings carry profound implications for precision medicine in Alzheimer’s disease. A one-size-fits-all biomarker framework may inadvertently overlook distinctive pathophysiological mechanisms encountered in different ethnoracial groups. Consequently, clinical trials, diagnostic criteria, and therapeutic strategies must be recalibrated to accommodate biological variability shaped by genetic background, environment, and socio-cultural influences.

Importantly, the data advocate for longitudinal follow-up to dissect how tau, amyloid, vascular function, genetics—including the presence of the APOEε4 allele—and social determinants coalesce over time to influence cognitive trajectories. Such prolonged observation will be instrumental in unraveling the intricate web of contributory factors and optimizing prevention and intervention approaches tailored to diverse populations.

Moreover, the study’s revelations about non-amyloid influences on cognitive decline in Black adults spotlights the pressing need to investigate comorbid conditions and life-course exposures that may exacerbate or mimic Alzheimer’s symptoms. This integrative understanding is critical to avoid misdiagnosis and to design effective treatments that address the broader health context of patients.

The research team strongly advocates for the expansion of neuroimaging studies to encompass a wider array of communities historically underrepresented in Alzheimer’s research. Achieving true equity in neuroscientific inquiry will not only improve diagnostic sensitivity but also enhance the validity and generalizability of scientific findings, ultimately benefiting global populations afflicted by dementia.

In conclusion, this landmark study redefines the landscape of Alzheimer’s disease research by illustrating the heterogeneity in biomarker expression across ethnoracial groups. It challenges entrenched paradigms and sets the stage for a new era in which Alzheimer’s pathology is understood through the lens of diversity. Future efforts must continue to unravel these complex biological and social interdependencies to pave the way for personalized, equitable diagnostic and therapeutic solutions.

Subject of Research: People

Article Title: The relationships between ethnoracial identity, Aβ positivity, APOEε4, and medial temporal lobe tau PET

News Publication Date: 4-Mar-2026

Web References:

• Stevens INI
• Alzheimer’s & Dementia Journal Article
• HABS-HD Study
• Related Animation

References:
10.1002/alz.71226

Image Credits: USC/Stevens INI

Keywords: Alzheimer disease, Tau proteins, Amyloid hypothesis, Amyloidosis, Dementia, Human brain, Brain, Positron emission tomography