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Higher coffee consumption is associated with slower cognitive decline and Aβ‐amyloid accumulation over 126 months: Data from the AIBL study
Journal article   Peer reviewed

Higher coffee consumption is associated with slower cognitive decline and Aβ‐amyloid accumulation over 126 months: Data from the AIBL study

Samantha L Gardener, Stephanie R Rainey-Smith, Victor LL Villemagne, Jurgen Fripp, Vincent Dore, Pierrick Bourgeat, Kevin Taddei, Colin L Masters, Paul T Maruff, Christopher C Rowe, …
Alzheimer's & dementia: The Journal of the Alzheimer's Association, Vol.17(S10), e051574
2021

Abstract

Background Worldwide, coffee is one of the most popular beverages consumed. Several studies have suggested a protective role of coffee, including reduced risk of Alzheimer’s disease (AD). However, there is limited longitudinal data available in cohorts of older adults reporting associations of coffee intake with cognitive decline, in distinct domains, and investigating the neuropathological mechanisms underpinning these associations. Method The aim of the current study was to investigate the relationship between self-reported baseline coffee intake (mean = 280 ± 323 g/day) and cognitive decline assessed using a comprehensive neuropsychological battery, over 126 months, in 227 cognitively normal individuals from the Australian Imaging, Biomarkers, and Lifestyle (AIBL) study. We also sought to investigate the relationship between coffee intake and cerebral Aβ-amyloid accumulation and brain volumes in a subset of individuals (n=60; and n=51, respectively) over 126 months. Result Higher baseline coffee consumption was associated with slower cognitive decline in executive function, attention, and the AIBL Preclinical AD Cognitive Composite (PACC; shown to reliably measure the first signs of cognitive decline in at-risk cognitively normal populations) over 126 months. Higher baseline coffee consumption was also associated with slower Aβ-amyloid accumulation over 126 months, and lower risk of transitioning from ‘negative’ Aβ-amyloid status to ‘moderate’, and ‘very high’ Aβ-amyloid burden over the same time period. There were no associations between coffee intake and atrophy in total grey matter, white matter, or hippocampal volume. Conclusion Our results further support the hypothesis that coffee intake may be a protective factor against AD, with increased coffee consumption reducing cognitive decline potentially by slowing cerebral Aβ-amyloid accumulation, and thus attenuating the associated neurotoxicity from Aβ-amyloid-mediated oxidative stress and inflammatory processes. Further investigation is required to evaluate how coffee intake could be incorporated as one modifiable lifestyle factor aimed at delaying AD onset.

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