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O1‐02‐05: A novel positron emission tomography contrast agent targeting cathepsin d shows preferential in vivo retention in an Alzheimer's disease mouse model
Author(s) -
Snir Jonatan A.,
Suchy Mojmir,
Bindseil Geron A.,
Chronik Blaine A.,
Hudson Robert H.E.,
Pasternak Stephen H.,
Bartha Robert
Publication year - 2015
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.2015.07.037
Subject(s) - in vivo , cathepsin d , ex vivo , positron emission tomography , chemistry , genetically modified mouse , in vitro , preclinical imaging , microbiology and biotechnology , transgene , medicine , nuclear medicine , biochemistry , biology , enzyme , gene
(8465.76639.2 mm), while it was not significantly different in PDD subjects (7568.761095.4mm) compared to controls. [11C](R)PK11195 BP was significantly increased in all cortical ROIs in both AD and PDD subjects compared to controls; the regional cortical rCMRGlc was significantly reduced in AD and PDD compared to controls in almost all ROIs. SPM Correlation between [11C](R)PK11195 BP, rCMRGlc and hippocampal volume indicated that both in AD and PDD increased glial activation, as well as reduced glucose metabolism, show a negative and positive correlation, respectively, with hippocampal volume (Figure 1). The spatial agreement between local and distant glial activation in the cortical projections and atrophy in hippocampus supports the theory that chronically activated glial cells might be one of the effectors of neurodegenerative processes. Conclusions: We have shown that glial activation, as assessed by [11C](R)PK11195 PET, inversely correlates with hippocampal volume in neurodegenerative diseases with dementia, providing further evidence for the central role of microglial activation in neurodegenerative diseases like AD and PDD.