PET imaging is adding a new layer of understanding to scientists’ concept of Alzheimer’s disease pathogenesis and progression. At the 14th Human Amyloid Imaging conference, speakers detailed nuances in the relationship between plaques, tangles, and cognitive decline. They also described nascent efforts to tie pathology in specific brain regions to specific behavioral and cognitive symptoms. While HAI featured new data on the pros and cons of various tau tracers in development, the synaptic tracer UCB-J jumped to the fore. It appears to detect synapse loss throughout AD cortex, as well as in other neurodegenerative diseases such as frontotemporal dementia and progressive supranuclear palsy.
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.
At HAI 2020, scientists more precisely quantified the relationship between plaques, tangles, and cognitive decline.