Lewy body disease is defined by the abnormal accumulation of a protein called alpha-synuclein, associated with dysfunction and loss of brain cells over time. The protein builds up in deposits called Lewy bodies. But the brain rarely tells just one story. A significant number of people with Lewy body disease, as many as half or more, also carry the hallmarks of Alzheimer's disease at the same time — and that combination has important consequences.

Alzheimer's disease is defined by two types of abnormal protein buildup: amyloid plaques and tau tangles. When these accumulate alongside Lewy bodies, researchers call it co-pathology. Scientific research has shown that the presence of amyloid and Lewy bodies together is associated with a faster rate of cognitive decline, an earlier onset of dementia, and a shorter lifespan. Identifying who has amyloid co-pathology has real meaning for prognosis, care, and treatment.

A blood-based biomarker called pTau217 has already been established as a reliable diagnostic tool in Alzheimer's disease. When it is present, it indicates that amyloid and tau are both in the brain. But a critical question remained unanswered: does it remain reliable when Lewy body pathology is also present? The biological environment of a brain carrying both Lewy bodies and Alzheimer's pathology is different from one carrying Alzheimer's pathology alone. A biomarker that performs well in one setting cannot be assumed to perform equally well in the other. Until now, this question had not been rigorously tested.

A research team led by Drs. Kathleen Poston and Carla Abdelnour at Stanford University (an LBDA Research Center of Excellence), in collaboration with colleagues at the Sant Pau Memory Unit in Barcelona, set out to answer that question directly. Their study included 253 participants drawn from both institutions. The discovery phase used cerebrospinal fluid — the liquid surrounding the brain and spinal cord — to confirm both Lewy body pathology and amyloid status in research volunteers, creating a biologically grounded foundation for the analysis. In other words, they knew going into the study which volunteers had Lewy bodies, which had Alzheimer's pathology, and which had both. Researchers then measured plasma pTau217 alongside several other blood biomarkers to determine which performed best at detecting amyloid pathology in people who also had confirmed Lewy body pathology. The answer was clear: plasma pTau217 outperformed the other biomarkers, achieving a diagnostic accuracy of 0.92 on a scale where 1.0 is perfect. These findings held up when tested in two independent groups of people with clinically diagnosed Lewy body disease. (It is worth noting here that the volunteers were primarily non-Hispanic white, and further research is needed to confirm these findings extend across more diverse populations.)

This finding matters for two reasons. First, it is an important step toward having a minimally invasive tool for detecting Alzheimer's co-pathology in people with Lewy body disease — reducing the need for expensive imaging or spinal taps for many patients. But perhaps more significantly, it opens a door that has been difficult to push open: clinical trials of drugs targeting amyloid in people with Lewy body disease who have biomarker evidence of both pathologies. Anti-amyloid therapies have shown benefit in Alzheimer's disease, and there is strong scientific rationale for exploring whether they could also benefit the substantial number of people with Lewy body disease who also have Alzheimer's co-pathology.

While more research is needed, this represents real progress for early and accurate diagnosis and for clinical trials for people living with LBD. There is always a need for more research volunteers. If you may be interested in learning more, visit the LBDA clinical trials page. And to be notified when new studies launch, consider joining the Lewy Trial Tracker.

REFERENCE

Smith AM, Lorkiewicz SA, Arslan B et al. 2026. Plasma phosphorylated tau 217 detects amyloid-β in neuronal synuclein disease. npj Parkinsons Dis. DOI: 10.1038/s41531-026-01341-8