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O1–03–02: In vivo targeting of antibody fragments to the nervous system for Alzheimer's disease immunotherapy and molecular imaging of amyloid plaques
Author(s) -
Poduslo Joseph F.,
Holasek Silvina S.,
Ramakrishnan Muthu,
Ramirez-Alvarado Marina,
Gilles Emily J.,
Curran Geoffry L.,
Wengenack Thomas M.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.045
Subject(s) - antibody , in vivo , polyamine , genetically modified mouse , central nervous system , antigen , chemistry , pathology , transgene , monoclonal antibody , microbiology and biotechnology , medicine , immunology , biology , biochemistry , neuroscience , gene
formed. Results: Increased [11C](R)-PK11195 binding in AD was found in medial inferior frontal lobe, medial inferior temporal lobe, entorhinal cortex, posterior cingulate cortex and occipital lobe. In MCI the medial temporal lobe and, more specifically, the entorhinal cortex showed increased binding. However, BP did not allow for differentiation between converters or non-converters. SPM analysis showed increased binding in lateral temporal and occipital lobes in both MCI and AD. Discussion: The distribution of increased [11C](R)-PK11195 binding in MCI and AD agrees with areas known to be affected pathologically in AD and supports the theory that inflammation might be an early phenomenon in the etiology of AD. Although this ligand might lack sensitivity for diagnostic purposes in individual patients, it could be useful for addressing changes in [11C](R)-PK11195 binding (e.g., due to therapy) at a group level.