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P1‐305: CORTICAL BURDEN OF AMYLOID BETA AND PHF TAU IN DEMENTED AND NON‐DEMENTED INDIVIDUALS
Author(s) -
Postupdia O.,
Hewitt Jessica L.,
Sonnen Joshua A.,
Larson Eric Berg,
Crane Paul K.,
Keene C. Dirk,
Montine Thomas J.
Publication year - 2014
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.2014.05.546
Subject(s) - dementia , pathological , pathology , cohort , alzheimer's disease , amyloid (mycology) , cortex (anatomy) , disease , pathophysiology , apolipoprotein e , medicine , temporal cortex , beta (programming language) , psychology , neuroscience , computer science , programming language
mutual complaint evidenced more diffuse amyloid plaques (OR1⁄46.8, p1⁄40.01), a trend for a higher BRAAK stage (OR1⁄43.0, p1⁄40.086), and a trend to meet NIA/Reagan (OR1⁄43.2, p1⁄40.068) and CERAD criteria (OR1⁄43.7, p1⁄40.09). In a secondary analysis, logistic regression related the combination of AD and vascular pathology (using ’vascular pathology only’ as the referent) to the presence of any complaint prior to death (self, informant, and mutual), yielding a significant observation (OR1⁄47.2, p1⁄40.006). Conclusions: MCI individuals with a mutual (both selfand informant-) complaint are more likely to have AD pathology at death than their peers with no-complaint. This finding is consistent with research suggesting mutual complaint is most predictive of cognitive trajectory and conversion. Additionally, MCI individuals with concomitant vascular and AD pathology are more likely to have some type of cognitive complaint than their peers with only vascular pathology. Funding: R01-HL11516, R01-AG034962, K12-HG043483, NIRG-13-283276, K24-AG046373, U01-AG016976.