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Comparison of amyloid plaque contrast generated by T 2 ‐weighted, T   2 * ‐weighted, and susceptibility‐weighted imaging methods in transgenic mouse models of Alzheimer's disease
Author(s) -
Chamberlain Ryan,
Reyes Denise,
Curran Geoffrey L.,
Marjanska Malgorzata,
Wengenack Thomas M.,
Poduslo Joseph F.,
Garwood Michael,
Jack Clifford R.
Publication year - 2009
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.21951
Subject(s) - ex vivo , susceptibility weighted imaging , quantitative susceptibility mapping , genetically modified mouse , magnetic resonance imaging , gradient echo , in vivo , cortex (anatomy) , pathology , nuclear magnetic resonance , chemistry , biology , transgene , neuroscience , medicine , physics , biochemistry , microbiology and biotechnology , radiology , gene
One of the hallmark pathologies of Alzheimer's disease (AD) is amyloid plaque deposition. Plaques appear hypointense on T 2 ‐weighted and T   2 * ‐weighted MR images probably due to the presence of endogenous iron, but no quantitative comparison of various imaging techniques has been reported. We estimated the T 1 , T 2 , T   2 * , and proton density values of cortical plaques and normal cortical tissue and analyzed the plaque contrast generated by a collection of T 2 ‐weighted, T   2 * ‐weighted, and susceptibility‐weighted imaging (SWI) methods in ex vivo transgenic mouse specimens. The proton density and T 1 values were similar for both cortical plaques and normal cortical tissue. The T 2 and T   2 *values were similar in cortical plaques, which indicates that the iron content of cortical plaques may not be as large as previously thought. Ex vivo plaque contrast was increased compared to a previously reported spin‐echo sequence by summing multiple echoes and by performing SWI; however, gradient echo and SWI were found to be impractical for in vivo imaging due to susceptibility interface–related signal loss in the cortex. Magn Reson Med, 2009. © 2009 Wiley‐Liss, Inc.

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