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P1‐433: decreased CSF amyloid beta 38, 40 and 42 in genetically and pathologically confirmed FTD

N. Verwey, C. Teunissen, J. Hoozemans, A. Rozemuller, P. Scheltens, Y. Pijnenburg

Alzheimer's & Dementia, 2019

468 participants

Abstract

Background: In previous studies we observed protective associations of dietary intakes of flavonols with Alzheimer’s dementia and cognitive decline. In this study, we investigated the associations of total flavonol intake and its constituents (kaempferol, quercetin, myricetin, and isorhamnetin) to the burden of Alzheimer’s disease neuropathology in a large community-based cohort study.Methods: Dietary intakes of flavonols obtained through food frequency questionnaires pre-mortem were related to post-mortem brain measures of AD neuropathology among 468 deceased participants of the Rush Memory and Aging project (MAP). Neuropathological outcomes included global burden of AD neuropathology, average cortical amyloid load, neurofibrillary tangle density, NIA-Reagan score (likelihood of AD diagnosis), Braak stage (semiquantitative measure of neurofibrillary tangle spread and severity), and CERAD score (semiquantitative score of neuritic plaques). We used linear and logistic regression models to examine associations of tertiles of energy-adjusted intakes of flavonols with the neuropathologic outcomes. Results: In separate linear regression models adjusted for age, sex, and education (basic model), the highest tertile versus lowest tertile of total flavonol intake was significantly associated with a lower global AD pathology (b1⁄4 -0.31 SE 1⁄4 0.14, p value1⁄4 0.03), average amyloid burden (b1⁄4 -0.67, SE1⁄4 0.25, p1⁄4 0.008) and CERAD score (b1⁄4 -0.26, SE1⁄40.13, p1⁄4 0.04). In…

How strong is the evidence?

Evidence Hub reads this as a cohort study, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 468 participants or records.

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