Lecanemab slows progression of novel Alzheimer’s-related biomarker over 18 months
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Key takeaways:
- Lecanemab led to a 44% reduction of biomarker MTBR-tau243 at 18 months.
- MTBR-tau243 levels increase over time and track with changes in tau positron emission tomography.
PHILADELPHIA — Treatment with lecanemab slowed the progression of a potential novel Alzheimer’s disease-related biomarker by 44% over 18 months compared with placebo, with the biomarker itself most correlating with tauopathy, data show.
“Lecanemab has a dual action,” Kristin R. Wildsmith, PhD, senior director of Clinical Pharmacology and Translational Medicine in the Neurology Business Group at Eisai, said during her presentation at the Alzheimer’s Association International Conference. “By blocking the amyloid cascade, it is, in turn, also slowing the tau cascade.”
Prior data from the CLARITY AD clinical trial established that individuals in the early stages of Alzheimer’s disease (AD) treated with lecanemab (Leqembi, Eisai) are progressing slower on tau-based positron emission tomography (PET) compared with placebo.
Wildsmith and colleagues analyzed cerebrospinal fluid (CSF) from a subset of participants from CLARITY AD in either the treatment or placebo groups by using C2N Diagnostics’ IP_MS assay.
They sought to determine whether MTBR-tau243 was reliable as a possible biomarker surrogate for tau-related pathology, to assess changes from baseline in MTBR-tau243 trajectory in the placebo group and to compare that trajectory in placebo vs. lecanemab to evaluate effects of treatment.
Of the 1,734 participants in CLARITY AD, 167 were included in the subset analysis, 84 of whom were assigned to lecanemab (mean age, 71.4 years; 53.6% women) and 83 to placebo (mean age, 69.6 years; 62.7% women).
According to the results, treatment with lecanemab resulted in a 44% slowing of the MTBR-tau243 compared with placebo at 18 months.
Additionally, data showed that increase tracked with changes in tau PET compared with amyloid PET.
The researchers also found that levels of MTBR-tau243 increased over the course of CLARITY AD, with the subset analysis confirming a higher correlation at baseline with tau PET compared with amyloid PET.
“This biomarker increases over time and tracks with changes in tau PET,” Wildsmith noted. “And lecanemab seems to slow the progression of not only MTBR-tau243 but also tau PET.