![]() More signal tracked with better scores on the CDR-SB and on a measure of episodic memory. Overall, the findings match the pattern of synaptic loss seen in postmortem AD brain.Īnd UCB-J binding mattered. The uncorrected signal probably represents the total number of synapses in the region, while the corrected one indicates synaptic density in the remaining tissue both are potentially interesting, van Dyck told Alzforum. After correcting for brain atrophy, the signal remained significant in the hippocampus and amygdala, as well as in the entorhinal, lateral temporal, parietal, pericentral, and prefrontal cortex. The differences were biggest in the hippocampus and entorhinal cortex, but were statistically significant across the board. In every brain region examined, amyloid-positive people bound less tracer than did controls (see image above, part A). Using this method, Mecca and colleagues scanned 19 cognitively normal controls, 14 people with mild cognitive impairment due to AD, and 20 with AD dementia. There, tracer uptake was less variable from person to person, lowering noise and sharpening the signal. Instead of using the centrum semiovale, a patch of white matter above the lateral ventricles, as the reference region, the researchers turned to the cerebellum. ![]() In Miami, Adam Mecca of Yale described how the methodology for analyzing the UCB-J signal had improved. ![]() ĭwindling Synaptic Signal Flags Alzheimer’s Disease More Amyloid, Fewer Synapses. In healthy people (left), the synaptic PET signal (top) is high, while amyloid PET (bottom) is low in people with AD (right), the opposite is true. Some researchers in Miami reported decreased UCB-J uptake in frontotemporal dementia, Parkinson’s disease, and progressive supranuclear palsy, as well (see Part 2 of this series).ĭeveloped by the Belgian pharma company UCB and first tested at Yale, UCB-J binds to the presynaptic vesicle protein SV2A ( Jul 2016 news). In an initial study of 10 AD patients and 11 controls, van Dyck and colleagues found that patients took up less UCB-J than did controls in their hippocampus, though they were unable to see a difference in cortical regions ( Dec 2017 conference news Aug 2018 conference news). The same methods are shedding light on other neurodegenerative diseases. They are also beginning to collect longitudinal data and scan people at presymptomatic disease stages to find out when synapses start to disappear.īroadly speaking, studies increasingly combine imaging with multiple tracers, and these emerging data are helping scientists stage which biomarker changes follow others in the long process of Alzheimer’s pathogenesis. However, so far, few people have been scanned, and scientists are repeating the findings in larger cohorts. Overall, the emerging data strengthen the case that this tracer could be used to help diagnose Alzheimer’s disease, and perhaps even detect a slowing of synapse loss with treatment, researchers said. Other presentations at HAI linked decreased UCB-J signal to more plaques and tangles as seen by PET. In this study, lower UCB-J uptake also correlated with worse cognitive performance. “For the first time, we’re seeing with UCB-J PET in vivo what we expected to see based on the autopsy studies,” Christopher van Dyck of Yale University, New Haven, Connecticut, the senior author of the research, told Alzforum. It holds out the prospect of live imaging of a phenomenon that neuropathologists have been describing for many years. This new evidence of widespread loss in cortical regions broadly extends previous hints that the tracer, UCB-J, picks up synaptic loss in the hippocampi of AD patients. PET Tracer Detects Synapse Loss Across Alzheimer’s BrainĪ PET tracer that lights up synapses is able to detect a loss of connectivity across the Alzheimer’s brain, according to new research presented at the Human Amyloid Imaging conference, held January 15–17 in Miami, Florida. ![]() It appears to detect synapse loss throughout AD cortex, as well as in other neurodegenerative diseases such as frontotemporal dementia and progressive supranuclear palsy. 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. They also described nascent efforts to tie pathology in specific brain regions to specific behavioral and cognitive symptoms. 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. How would you like to share? Facebook Twitter LinkedIn
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