As methodology improves, the new tracer UCB-J reliably flags synapse loss in Alzheimer’s cortex, reported scientists at the Human Amyloid Imaging conference in Miami. Other speakers correlated UCB-J uptake with amyloid and tau PET and cognitive decline, strengthening the case for its use as an AD biomarker. The tracer also picks up dramatic synapse loss in frontotemporal dementia and progressive supranuclear palsy, and modest declines in early Parkinson’s disease.
New research presented at the HAI conference also finds links between UCB-J uptake and plaques, tangles, and cognitive decline.
Synapse loss and mitochondrial stress, as seen by separate PET tracers, go hand-in-hand in Alzheimer’s, Parkinson’s, and frontotemporal dementia.
At the HAI 2020 conference, the tracers PI-2620 and APN-1607 appeared to bind frontotemporal dementia tau. MK-6240 looked highly sensitive. And JNJ-067 and SNFT-1 are two new kids in town.
Amyloid and tau PET are helping scientists pinpoint the underlying cause of specific AD symptoms. Perhaps imaging of certain brain regions will help predict an individual’s progression.