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P1–260: Required features of a fluorine‐19 MRI probe for amyloid detection in the brain
Author(s) -
Yanagisawa Daijiro,
Taguchi Hiroyasu,
Morikawa Shigehiro,
Inubushi Toshiro,
Ibrahim Nor Faeizah,
Hirao Koichi,
Shirai Nobuaki,
Sogabe Takayuki,
Tooyama IKuo
Publication year - 2013
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.2013.05.485
Subject(s) - ethylene glycol , chemistry , peg ratio , magnetic resonance imaging , amyloid (mycology) , polyethylene glycol , amyloid precursor protein , molecular imaging , fluorescence microscope , biophysics , nuclear magnetic resonance , fluorescence , alzheimer's disease , biochemistry , pathology , medicine , in vivo , biology , disease , inorganic chemistry , physics , microbiology and biotechnology , organic chemistry , finance , quantum mechanics , economics , radiology
(Fe), copper (Cu), and zinc (Zn). The overall levels of these metals have been investigated in a variety of brain homogenates and extracts, unfortunately these analyses have provided little consensus on the importance of the overall levels in Alzheimer’s disease. While this is the case, specific regions of enrichment, or mis-localisation of metals in the Alzheimer’s disease brain are very important and by attenuating a specific metal such that it does not interact with Ab should provide a therapeutic benefit. Methods: Brain tissue samples of 18 month old PPSAPP mouse were used for this study. The localization of amyloid plaques was determined by staining the tissue sections with Thioflavin S. The concentration and distribution of trace elements in the brain tissue were measured with x-ray florescence microprobe. The experiments were carried out at beamline XFM at the Australian Synchrotron. Results: Using the PSAPP mouse model of cerebral amyloid plaque formation, we conducted a survey ofmetal ion content and distribution Ca, Fe, Cu, and Zn through the neocortex and hippocampus using XFM. We established that elastic scattering and differential phase contrast can be used to identify the location of plaques without the need for typical histological staining. Plaque metalliation levels varied in concert with the metal content of the surrounding neutrophil and within a given anatomical region was found to be highly uniform across many tens of aggregates. Conclusions: Since neuropathological changes in human Alzheimer’s disease are presumed to involve disturbances to metal physiology, quantification of statistical representative numbers of plaques without the need for staining before assay promises to provide insight into the pathogenesis of Alzheimer’s disease.

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