Ryan Coppens1,2, Norka E Rabinovich1, Raghuveer Kanneganti1, Herman A Diggs1,2, Kristin Wiggs1, Travis Healey3, Jodi Huggenvik3, Gregory M Rose2,3,4, David G Gilbert5,6,7. 1. Department of Psychology, Southern Illinois University, Carbondale, IL, USA. 2. Center for Integrated Research in Cognitive & Neural Sciences, Southern Illinois University, Carbondale, IL, USA. 3. Department of Physiology, Southern Illinois University School of Medicine, Springfield, IL, USA. 4. Department of Anatomy, Southern Illinois University School of Medicine, Springfield, IL, USA. 5. Department of Psychology, Southern Illinois University, Carbondale, IL, USA. dgilbert@siu.edu. 6. Center for Integrated Research in Cognitive & Neural Sciences, Southern Illinois University, Carbondale, IL, USA. dgilbert@siu.edu. 7. School of Psychological and Behavioral Sciences, Southern Illinois University, Mail Code 6502, Carbondale, IL, 62901, USA. dgilbert@siu.edu.
Abstract
RATIONALE: There is strong evidence that nicotine can enhance cognitive functions and growing evidence that this effect may be larger in young healthy APOE ε4 carriers. However, the moderating effects of the APOE ε4 allele on cognitive impairments caused by nicotine deprivation in chronic smokers have not yet been studied with brain indices. OBJECTIVE: We sought to determine whether young female carriers of the APOE ε4 allele, relative to noncarriers, would exhibit larger abstinence-induced decreases in P3b amplitude during a two-stimulus auditory oddball task. METHODS: We compared parietal P3bs in female chronic smokers with either APOE ε3/ε3 (n = 54) or ε3/ε4 (n = 20) genotype under nicotine-sated conditions and after 12-17-h nicotine deprivation. RESULTS: Nicotine deprivation significantly reduced P3b amplitudes in APOE ε4 carriers, but not in APOE-ε3/ε3 individuals, such that the difference seen prior to nicotine deprivation was eliminated. CONCLUSIONS: The results suggest that subjects with the APOE ε4 allele are more sensitive to nicotine, which could influence smoking patterns, the risk for nicotine dependence, and the cognitive effects of nicotine use in these individuals.
RATIONALE: There is strong evidence that nicotine can enhance cognitive functions and growing evidence that this effect may be larger in young healthy APOE ε4 carriers. However, the moderating effects of the APOE ε4 allele on cognitive impairments caused by nicotine deprivation in chronic smokers have not yet been studied with brain indices. OBJECTIVE: We sought to determine whether young female carriers of the APOE ε4 allele, relative to noncarriers, would exhibit larger abstinence-induced decreases in P3b amplitude during a two-stimulus auditory oddball task. METHODS: We compared parietal P3bs in female chronic smokers with either APOE ε3/ε3 (n = 54) or ε3/ε4 (n = 20) genotype under nicotine-sated conditions and after 12-17-h nicotine deprivation. RESULTS:Nicotine deprivation significantly reduced P3b amplitudes in APOE ε4 carriers, but not in APOE-ε3/ε3 individuals, such that the difference seen prior to nicotine deprivation was eliminated. CONCLUSIONS: The results suggest that subjects with the APOE ε4 allele are more sensitive to nicotine, which could influence smoking patterns, the risk for nicotine dependence, and the cognitive effects of nicotine use in these individuals.
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