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MRI assessment of neuropathology in a transgenic mouse model of Alzheimer's disease
Author(s) -
Helpern Joseph A.,
Lee SangPil,
Falangola Maria F.,
Dyakin Victor V.,
Bogart Adam,
Ardekani Babak,
Duff Karen,
Branch Craig,
Wisniewski Thomas,
de Leon Mony J.,
Wolf Oliver,
O'Shea Jacqueline,
Nixon Ralph A.
Publication year - 2004
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.20038
Subject(s) - presenilin , genetically modified mouse , neuropathology , amyloid precursor protein , hippocampus , retrosplenial cortex , corpus callosum , alzheimer's disease , transgene , senile plaques , pathology , neuroscience , amyloid (mycology) , hippocampal formation , medicine , endocrinology , biology , disease , gene , biochemistry
The cerebral deposition of amyloid β‐peptide, a central event in Alzheimer's disease (AD) pathogenesis, begins several years before the onset of clinical symptoms. Noninvasive detection of AD pathology at this initial stage would facilitate intervention and enhance treatment success. In this study, high‐field MRI was used to detect changes in regional brain MR relaxation times in three types of mice: 1) transgenic mice (PS/APP) carrying both mutant genes for amyloid precursor protein (APP) and presenilin (PS), which have high levels and clear accumulation of β‐amyloid in several brain regions, starting from 10 weeks of age; 2) transgenic mice (PS) carrying only a mutant gene for presenilin (PS), which show subtly elevated levels of Aβ‐peptide without β‐amyloid deposition; and 3) nontransgenic (NTg) littermates as controls. The transverse relaxation time T 2 , an intrinsic MR parameter thought to reflect impaired cell physiology, was significantly reduced in the hippocampus, cingulate, and retrosplenial cortex, but not the corpus callosum, of PS‐APP mice compared to NTg. No differences in T 1 values or proton density were detected between any groups of mice. These results indicate that T 2 may be a sensitive marker of abnormalities in this transgenic mouse model of AD. Magn Reson Med 51:794–798, 2004. © 2004 Wiley‐Liss, Inc.