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[ 11 C]PIB Retention A conventional explanation of the pathogenesis of AD is the A cascade, according to which increased production or decreased clearance of fibrillary A leads to loss of dendritic spines and symptoms of dementia ( 11 C]PIB than patients without the A deposits, and the binding correlates with amyloid deposits in brain tissue removed at autopsy ( In contrast, animal studies have shown significant changes in A load after treatment with the GLP-1 analog liraglutide ( 11 C]PIB binding no longer undergoes the increases seen in the animal models ( 11 C]PIB retention has not been demonstrated

[5] This extended duration of action made it an attractive candidate for therapeutic development

Retrograde transport from endosomes to the trans-Golgi network

These could be signs of a more serious problem like a blood clot