Leqembi and p-tau217: A Blood Test Offers a New Window Into Alzheimer’s
The Alzheimer’s Association recently highlighted a study that struck a direct chord with me: “Heterogeneity in plasma p-tau217 response and its association with cognitive trajectories under lecanemab treatment.” The study provides encouraging evidence that Leqembi (lecanemab) may do more than simply slow the clinical progression of Alzheimer’s disease, it may produce measurable biological changes that can be detected in the blood. The findings are not conclusive proof that a reduction in p-tau217 means Leqembi is working in every individual patient, but they certainly suggest an important potential additional benefit of treatment: we may be able to see evidence of the drug’s biological effect through a blood test. Hopefully, my own experience is an example of what the researchers are beginning to see.
I have been receiving Leqembi infusions since August 2024, and my blood testing has included measurements of the Alzheimer’s biomarker p-tau217. My results have changed considerably over the course of my treatment:
These are my results:
Date p-tau217 August 2024 0.410 April 2025 0.180 August 2026 0.140 According to the LabCorp reference range used for my testing, 0–0.18 is the reference range, with readings above 0.180 indicating a level associated with amyloid-related pathology. My first result, 0.410, was therefore well above that range. By April 2025, after approximately eight months of Leqembi treatment, my level had fallen to 0.180. By August 2026, it had fallen further to 0.140, now within the laboratory's reference range.
That does not prove that Leqembi alone caused these changes. There are many factors that can influence an individual's biomarkers, and one person's experience cannot establish cause and effect. But the pattern is certainly encouraging, particularly when viewed alongside the findings of the new study.
What the researchers found
Doctors are beginning to have a way to look for biological evidence that an Alzheimer’s treatment is changing the disease process, rather than having to wait years to determine whether a person's memory and thinking decline.
In this study, researchers followed people with early Alzheimer’s disease who were being treated with lecanemab (Leqembi). They repeatedly measured a substance in the blood called p-tau217. This biomarker reflects changes associated with both amyloid and tau, two of the major biological features of Alzheimer’s disease.
The researchers found that p-tau217 began falling as early as three months after treatment began. The largest decline occurred between three and six months, after which the levels generally leveled off. In other words, the blood test appeared to provide an early indication that something biologically important was happening after treatment began.
But there was another important finding: patients did not all respond in the same way. Some experienced a much larger reduction in p-tau217 than others. Those with the greater reduction tended to have more favorable cognitive trajectories, including slower progression on the CDR-SB measure of cognitive and functional impairment.
This is particularly interesting to me because my own p-tau217 measurements show a substantial decline—from 0.410 before or around the beginning of my Leqembi treatment to 0.180 and then 0.140. My results are only one person's experience and cannot demonstrate that Leqembi caused the decline. Nevertheless, the direction of change is consistent with the biological pattern reported in this study.
Why would p-tau217 fall?
The researchers believe the answer may lie in the way Alzheimer’s disease develops.
Leqembi is designed to remove amyloid from the brain. Amyloid appears to respond earlier to anti-amyloid treatment than the more established tau pathology. Because p-tau217 reflects both amyloid and tau-related changes, an early decline in p-tau217 may partly reflect the reduction in amyloid-related disease activity produced by treatment.
The researchers also observed that p-tau217 tended to level off after about six months. One possible explanation is that while amyloid can be reduced by anti-amyloid treatment, established tau pathology may be more difficult to change and may respond more slowly. In that sense, the blood test may be giving researchers a glimpse into different stages of the disease process.
Not everyone responds the same way
The study found substantial differences among patients. Those whose p-tau217 levels fell more dramatically tended to experience more favorable cognitive trajectories. This raises an intriguing possibility: perhaps a blood test could eventually help doctors determine who is responding biologically to treatment and who is not.
That could be an important advance. Today, evaluating whether an Alzheimer’s treatment is helping largely involves watching a person's symptoms and cognitive performance over time. But symptoms can change slowly, and it may take a considerable period before a difference becomes apparent.
A biomarker such as p-tau217 offers another window. Instead of asking only, “How is the patient doing?” doctors may eventually be able to ask, “What is happening biologically?”
Other factors may matter
The researchers also found that hypertension was associated with a smaller reduction in p-tau217. They suggest that vascular problems may interfere with the brain's ability to clear amyloid and may also be associated with greater underlying tau pathology. Younger age was also associated with a smaller reduction in p-tau217, although the reasons for this finding remain uncertain.
These findings reinforce an important point: Alzheimer’s disease is not exactly the same disease in every person. A person's vascular health, age, underlying pathology, and other biological factors may influence how well a treatment works.
What my results mean to me
I don't know whether my declining p-tau217 levels mean that Leqembi is working exactly as the researchers describe. My results alone cannot answer that question.
But the possibility is significant.
I began Leqembi treatment in August 2024 with a p-tau217 level of 0.410. By April 2025, it had fallen to 0.180. By August 2026, it had fallen again to 0.140.
That is not a clinical trial. It is not proof. It is my experience.
But when I place those numbers beside this new research, I see a reason for optimism. The researchers are finding that some people receiving Leqembi experience substantial reductions in p-tau217 and that those reductions may be associated with a slower progression of cognitive impairment.
For someone actually living through Alzheimer’s disease, that possibility is more than an academic finding. It offers the hope that we may eventually be able to measure, through a simple blood test, whether a treatment is changing the underlying biology of the disease, not merely whether the symptoms have become worse.
And for me, seeing my own p-tau217 number move from 0.410 to 0.140 while receiving Leqembi is certainly encouraging.
The researchers themselves caution that much more work is needed. Their study was relatively small, conducted at a single center, and had a limited follow-up period. They also did not have direct measurements of tau deposits, such as tau PET imaging, to determine exactly how underlying tau pathology differed among patients.
Still, their conclusion points toward an important future for Alzheimer’s treatment: blood biomarkers such as p-tau217 may eventually help doctors see how individual patients are responding to disease-modifying treatments and make treatment more personalized.
For now, I can only say this: my numbers are moving in the direction I hope they are moving, and the research gives me a scientific reason to be encouraged.
References
Kang SH, P. Y. (2026, July 31). Heterogeneity in plasma p-tau217 response and its association with cognitive trajectories under lecanemab treatment. Retrieved from Alzheimer's Association: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.71705