ArticleThe pharmacogenomics journal2013
APOE ɛ4, an Alzheimer's disease susceptibility allele, and smoking cessation.
Article in The pharmacogenomics journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- A scoping review of smoking cessation pharmacogenetic studies to advance future research across racial, ethnic, and ancestral populations.Frontiers in genetics · 2023Article
- APOE genotype influences P3b amplitude and response to smoking abstinence in young adults.Psychopharmacology · 2021Article
- APOE e4 genotype and cigarette smoking in adults with normal cognition and mild cognitive impairment: a retrospective baseline analysis of a national dataset.The American journal of drug and alcohol abuse · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Possessing an apolipoprotein E (APOE) ɛ4 allele, advanced age and smoking are risk factors for Alzheimer's disease and cognitive decline. Deficits in cognitive function also increase risk for smoking relapse. Data from 917 adult smokers of European ancestry were pooled across three randomized trials of smoking cessation. We examined whether smokers who carry at least one ɛ4 allele (n=252) have more difficulty quitting smoking compared with noncarriers (n=665), and whether age moderated this association. The genotype by age interaction was significant for 7-day point-prevalence abstinence rates (P=0.04) and time to 7-day failure (P=0.03). Among smokers over age 60, ɛ4 carriers were less likely to quit (odds ratio=0.27, P=0.018) and relapsed more quickly (hazard ratio=3.38, P=0.001) compared with noncarriers. The genotype association with relapse was nonsignificant among younger smokers. An increased understanding of the underlying pathophysiological mechanisms of this association could facilitate the development of targeted therapies for smokers with increased risk for cognitive decline.
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Registered trials
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