We are pleased to announce the publication of top-line results from our HEAD study, on the comparison of tau PET tracers for the detection of tau pathology in Alzheimer’s disease, out now online in The Lancet.
We are grateful to our collaborators on this work, and we look forward to continuing the dissemination of our findings from this large-scale PET comparison study.
https://t.co/iNYnsMORE0
In cognitively unimpaired Aβ+ adults, MK6240 detected medial temporal tau in 39% of participants vs 16% with flortaucipir. That's a prevalence ratio of 2.43, which translates to 23 additional cognitively unimpaired Aβ+ individuals identified as tau-positive per 100 scanned.
MK6240 was significantly better at distinguishing Alzheimer's disease from non-Alzheimer's causes of impairment. AUC 0.93 vs 0.86 for Flortaucipir. Differences were largest in the medial temporal lobe, where early tau accumulates first.
Tau PET is central to Alzheimer's diagnosis and trial selection. But does tracer choice matter? The HEAD study set out to answer that. 682 participants, both Flortaucipir and MK6240, across the Alzheimer's spectrum. Out today in @TheLancet.
Article link: https://t.co/BUCVevtJJ0
🧠 New paper out in Nature Communications from the Karikari Lab @PittPsychiatry!
Led by Dr. @TommyKakari, our team,@Yijun8643878478 , Xuemei Zeng & Anirudh Sehrawat, plus Pitt collaborators Drs. Kang, Pascoal, Villemagne & Cohen, developed the streamlined PAβ V2.0 assay: faster, lower-volume & more accurate blood-based Alzheimer's biomarker detection. 🎉
📖 https://t.co/MYhM7j1VTR
#AlzheimersResearch #Biomarkers #NatureCommunications
We are thrilled that Dr. Pascoal was honored with the prestigious A.E. Bennett Award by the Society of Biological Psychiatry for his outstanding clinical contributions!
When focusing on individuals with intermediate Aβ levels, effect sizes increase and required sample sizes drop in both cognitively unimpaired and impaired groups—substantially reducing trial costs. These results support plasma p-tau217 as an efficient endpoint for AD trials.
Led by @pamlukasewicz, this multi-cohort study shows that longitudinal changes in plasma p-tau217 represent a robust endpoint for Alzheimer’s disease clinical trials.
https://t.co/Fmyd7mBhHB
We were very happy to receive Etienne Vachon-Presseau @evp82, Associate Professor at McGill, for a lab visit today! Etienne presented findings from analysis of UK Biobank data on prediction of chronic pain, including results from his group's recent papers (https://t.co/ZZuGrHDeSO).
Thank you for the visit, Etienne!
📌 Implication: Clinical trials targeting neuroinflammation in AD could benefit from stageing participants by Aβ and tau status as inflammation can lead to opposite effects depending on the disease stage.
In our new paper, we show that neuroinflammation in Alzheimer’s follows a two-wave pattern of harmful effects:
1️⃣ First wave: triggered by amyloid-β (Aβ)
2️⃣ Second wave: driven by widespread tau pathology
📄 https://t.co/3pHhKzBfjz
Importantly, neuroinflammation alone did not predict degeneration. Its detrimental effects appeared only in the presence of Aβ or tau pathology, suggesting a context-dependent role.
In our new study @NatureComms, Dr Soares et al show that CSF total tau, often used as a marker of neurodegeneration, is more strongly linked to synaptic degeneration than axonal or neuronal loss in Alzheimer’s disease.
Check our paper here🔗https://t.co/AP74CkgmsX