Association study in Alzheimer’s disease of single nucleotide polymorphisms implicated with coffee consumption

Abstract

Background: There is evidence from animal and in vitro models of the protective effects of caffeine in Alzheimer's disease. The suggested mechanisms through which caffeine may protect neurons against Alzheimer's disease pathology include the facilitation of beta-amyloid clearance, upregulation of cholinergic transmission, and increased neuronal plasticity and survival. Epidemiological studies support that Alzheimer's disease patients consume smaller amounts of coffee beverages throughout their lives as compared to age-matched cognitively healthy individuals. Objective: The aim of the present study was to determine whether the negative association between Alzheimer's disease and coffee consumption may be influenced by a common genetic predisposition, given the fact that the pattern of coffee consumption is determined by both environmental and genetic factors. Method: We conducted an in silico search addressing the association between genetic polymorphisms related to coffee consumption and the diagnosis of Alzheimer's disease. We further investigated the interactions between genes located in regions bearing these polymorphisms. Results: Our analysis revealed no evidence for a genetic association (nor interaction between related proteins) involving coffee consumption and Alzheimer's disease. Discussion: The negative association between Alzheimer's disease and coffee consumption suggested by epidemiological studies is most likely due to environmental factors that are not necessarily regulated by genetic background.

APOE Genotype and Alzheimer’s Disease: The Influence of Lifestyle and Environmental Factors

“…In this study, the APOE4 status did not affect the relationship of coffee intake with amyloid-beta positivity. In agreement with this evidence, an in silico analysis revealed no correlation between APOE polymorphisms related to coffee consumption and AD diagnosis, indicating that there is likely no strong impact of the APOE4 allele on the effect of coffee on AD risk …”

“…In agreement with this evidence, an in silico analysis revealed no correlation between APOE polymorphisms related to coffee consumption and AD diagnosis, indicating that there is likely no strong impact of the APOE4 allele on the effect of coffee on AD risk. 114 3.8. Alcohol Consumption.…”

Gene Expression Profiling in the Striatum of Per2 KO Mice Exhibiting More Vulnerable Responses against Methamphetamine

“…Consistently, Ncald expression was lower in patients with Alzheimer’s disease ( Shimohama et al ., 1996 ; Miller et al ., 2013 ). Ncald is also associated with coffee and caffeine consumption ( Yamamoto et al ., 2015 ; Lee, 2018 ). Ncald is one of the SNPs associated with coffee consumption.…”

Gender and ethnicity modify the association between the CYP1A2 rs762551 polymorphism and habitual coffee intake: evidence from a meta-analysis

“…The following papers were excluded: four GWAS (Cornelis et al, 2011;Sulem et al, 2011;Amin et al, 2012;Rodenburg et al, 2012); four studies lacking coffee intake analysis (Sachse et al, 1999;Basvi et al, 2007;Ghotbi et al, 2007;Gunes et al, 2009); eight studies not providing coffee intake data according to rs762551 genotypes (Goodman et al, 2003;Kotsopoulos et al, 2009;Hallström et al, 2010;Schmidt et al, 2010;Guessous et al, 2012;Josse et al, 2012;Palatini et al, 2015;Yamamoto et al, 2015); two studies providing CC and combined AC + AA genotypes counts instead of AA and AC + CC genotype counts (Palatini et al, 2009;Pavanello et al, 2010); two studies using patient samples (Cornelis et al, 2007;Bågeman et al, 2008); and one study with a small sample size . Finally, 12 studies were included in the meta-analysis (Nordmark et al, 2002;Sata et al, 2005;Cornelis et al, 2006;Kotsopoulos et al, 2007;Tan et al, 2007;Jernström et al, 2008;Djordjevic et al, 2010;Popat et al, 2011;Kohno et al, 2013;Lowcock et al, 2013;Tian et al, 2013;Dik et al, 2014) (Figure 1).…”