AstraZeneca presented the preclinical data on [18F]AZD4694 at the 9th International AD/PD meeting in Prague. In our preclinical studies, AZD4694 shows high affinity to amyloid plaque with very low non-specific interactions with white matter regions devoid of amyloid plaque. This low non-specific background provides a higher contrast and should support the potential to detect very low levels of amyloid. AZD4694 is currently in a Phase 1 study (in collaboration with Karolinska Institutet, Stockholm) with the objective to test clinical utility of this ligand. Our first data look very promising. We are supportive of ADNI, which has already made significant contributions to the field, and we have planned to make our ligand available for the sites in ADNI 2. The elegant study by Rosen et al., 2009, showing that PIB may be selective for pathological human-specific conformation of aggregated Aβ, indicates that we should be cautious when comparing results from different methods for evaluating Aβ plaque load in vitro (i.e., in vitro PET tracer...  Read more

AstraZeneca presented the preclinical data on [18F]AZD4694 at the 9th International AD/PD meeting in Prague. In our preclinical studies, AZD4694 shows high affinity to amyloid plaque with very low non-specific interactions with white matter regions devoid of amyloid plaque. This low non-specific background provides a higher contrast and should support the potential to detect very low levels of amyloid. AZD4694 is currently in a Phase 1 study (in collaboration with Karolinska Institutet, Stockholm) with the objective to test clinical utility of this ligand. Our first data look very promising. We are supportive of ADNI, which has already made significant contributions to the field, and we have planned to make our ligand available for the sites in ADNI 2. The elegant study by Rosen et al., 2009, showing that PIB may be selective for pathological human-specific conformation of aggregated Aβ, indicates that we should be cautious when comparing results from different methods for evaluating Aβ plaque load in vitro (i.e., in vitro PET tracer binding, ELISA for insoluble Aβ, and IHC). The data from Rosen et al. suggest that one should include PIB or another amyloid selective PET tracer when evaluating plaque load in vitro, to support translation to the in-vivo situation. Clearly more work is needed to unravel the molecular mechanism of amyloid ligand binding.

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