Rayna B Hirst1, Joshua T Jordan2,3, Sophia Miryam Schüssler-Fiorenza Rose4, Logan Schneider2,5,6,7, Makoto Kawai2,5,6,7, Christine E Gould2,8, Lauren Anker2,7, Christina F Chick2,7, Sherry A Beaudreau2,7, Joachim Hallmayer2,7, Ruth O'Hara2,5,7. 1. Department of Psychology, Palo Alto University, Palo Alto, CA, USA. 2. Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA. 3. Department of Psychiatry, University of California, San Francisco, CA, USA. 4. Department of Genetics, Stanford University, Stanford, CA, USA. 5. Stanford/VA State of California Alzheimer's Disease Research Center, VA Palo Alto Health Care System, Palo Alto, CA, USA. 6. Stanford University Sleep Center, Stanford University, Redwood City, CA, USA. 7. Sierra Pacific Mental Illness Research, Education, and Clinical Center (MIRECC), VA Palo Alto Healthcare System, Palo Alto, CA, USA. 8. Geriatric Research, Education and Clinical Center (GRECC), VA Palo Alto Health Care System, Palo Alto, CA, USA.
Abstract
OBJECTIVES: The short form or s-allele variant of the serotonin transporter polymorphism (5-HTTLPR), as compared with the long-form or l-allele variant, has been associated with the presence of cognitive dysfunction, and particularly memory impairment in older adults. This body of cross-sectional work has culminated in the hypothesis that presence of the s-allele predicts greater memory decline in older adults. Yet, to date, there are no longitudinal studies that have investigated this issue. METHODS/ DESIGN: Here, we examine 109 community-dwelling older adults (mean and SD of age = 70.7 ± 8.7 years) who underwent blood draw for genotyping, cognitive, and psychological testing at baseline, 12-, and 24-monthfollow-ups. RESULTS: Multilevel modeling found that s-allele carriers (ss or ls) performed worse than ll homozygotes at baseline on delayed verbal recall. Yet, s-allele carriers' memory performance was stable over the two-yearfollow-up period, while l-allele homozygotes experienced significant memory decline. l-allele homozygote status was associated with both increased cortisol and decreased memory over time, resulting in attenuated verbal memory performance differences compared to s-allele carriers with age. CONCLUSIONS: Overall, our findings do not support the hypothesis that presence of the 5-HTTLPRs-allele is a marker for memory decline in older adults. J Am Geriatr Soc 68:-, 2020.
OBJECTIVES: The short form or s-allele variant of the serotonin transporter polymorphism (5-HTTLPR), as compared with the long-form or l-allele variant, has been associated with the presence of cognitive dysfunction, and particularly memory impairment in older adults. This body of cross-sectional work has culminated in the hypothesis that presence of the s-allele predicts greater memory decline in older adults. Yet, to date, there are no longitudinal studies that have investigated this issue. METHODS/ DESIGN: Here, we examine 109 community-dwelling older adults (mean and SD of age = 70.7 ± 8.7 years) who underwent blood draw for genotyping, cognitive, and psychological testing at baseline, 12-, and 24-monthfollow-ups. RESULTS: Multilevel modeling found that s-allele carriers (ss or ls) performed worse than ll homozygotes at baseline on delayed verbal recall. Yet, s-allele carriers' memory performance was stable over the two-yearfollow-up period, while l-allele homozygotes experienced significant memory decline. l-allele homozygote status was associated with both increased cortisol and decreased memory over time, resulting in attenuated verbal memory performance differences compared to s-allele carriers with age. CONCLUSIONS: Overall, our findings do not support the hypothesis that presence of the 5-HTTLPRs-allele is a marker for memory decline in older adults. J Am Geriatr Soc 68:-, 2020.
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