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P4‐226: SOCIAL BEHAVIOR OF THE TRIPLE‐TRANSGENIC MOUSE MODEL OF ALZHEIMER'S DISEASE
Author(s) -
Sulkowski Brittany A.,
Rohr Benjamin V.,
Kasra John F.,
Wrenn Craige C.
Publication year - 2018
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.2018.07.047
Subject(s) - psychology , preference , developmental psychology , audiology , task (project management) , disease , social behavior , social recognition , neuroscience , social psychology , pathology , medicine , management , economics , microeconomics
deposition differed across the three mouse lines. APPswe/PS1dE9 mice accumulated plaques earliest, primarily in the isocortex in layers 2/3 and 5. hAPP-J20 mice had the most plaques in the hippocampus and retrosplenial cortex. Tg2576 mice had more vascularassociated plaques, with heavy accumulation in the subiculum. All three lines had dense plaques in the amygdala. Previous studies found that misfolded tau can increase the severity of Ab pathology, so to determine the impact of pathological tau on brain-wide Ab deposition patterns, we crossed APPswe/PS1dE9 mice with the rTg4510 tauopathy model. These mice had aggressive plaque deposition with a spatial pattern like the APPswe/PS1dE9 line. They also had more severe atrophy and cortical thinning than observed in either line alone, consistent with a synergistic role of Ab and tau in the development and progression of AD pathology. Conclusions:The three AD mouse models analyzed here have differential spatial and temporal patterns of plaque deposition brain-wide. Whole brain imaging of pathologies may thus provide critical information for whether a given model captures different aspects of AD pathologies. Future work will explore whether the Ab patterns observed are related to pathological alterations in network activity.