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Background: Uptake of amyloid imaging agents by specifically binding to amyloid protein in the human brain is compromised by a relatively weak target to background ratio in the range of 3 to 1. Blood brain permeability may be a limitation to improved target to background signal. We tested the ability of a novel blood-brain permeability peptide, termed K16ApoE, to enhance uptake of C11 (Pittsburgh Compound B) PiB in animal models of Alzheimer's disease (AD).
Methods: AD mice (APP/PS1) (n= 12) and wild type (WT) mice (N=13) were imaged with C11 PiB PET dynamically with K16ApoE and without. Quantitation using SUV measurements of PET uptake in brain, liver and heart was performed. Mice were then sacrificed and autoradiography of brain tissue was performed to assess the quantitative uptake measured in digital light units (DLU). Analysis was performed to compare brain-uptake of PiB on PET and on autoradiography with and without K16ApoE.
Results: Brain uptake of C11 PiB on PET was enhanced 3 fold in AD mice when delivered with K16APoE at early perfusion phase and 6 fold at 40 minutes (Figure 1; p = 0.01). The degree of enhancement in AD mice on PET was similar to that seen in WT. No enhancement of PiB uptake was seen in heart or liver on PET. Autoradiography confirmed a 20-fold increase in specific brain retention of PiB in amyloid carrying mice when delivered with K16APoE.
Conclusions: Enhancement of C11 PiB uptake in AD mice on PET imaging occurs by using blood brain barrier permeability enhancement with a novel blood-brain permeability peptide. This model could allow for more sensitive imaging of human brain amyloid in the future.