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An Immune Risk Phenotype, Cognitive Impairment, and Survival in Very Late Life: Impact of Allostatic Load in Swedish Octogenarian and Nonagenarian Humans

¹ Department of Natural Science and Biomedicine, School of Health Sciences, Jönköping University, Sweden.
² Department of Veterinary Science, College of Agricultural Sciences, The Pennsylvania State University, University Park.
³ Unilever Corporate Research, Colworth House, Sharnbrook, United Kingdom.
⁴ Department of Microbiology, Hospital of Ryhov, Jönköping, Sweden.
⁵ Department of Infectious Diseases, Hospital of Ryhov, Jönköping, Sweden.
⁶ Division of Clinical Immunology, Department of Health and Environment, University Hospital, Linköping, Sweden.
⁷ University of Tubingen Medical School, Center for Medical Research, Germany.
⁸ Institute of Gerontology, School of Health Sciences, Jönköping University, and Department of Psychology, Göteborg University, Sweden.

Address correspondence to Boo Johansson, Department of Psychology, Göteborg University, Box 500, 405 30 Göteborg, Sweden. E-mail: boo.johansson{at}psy.gu.se

In the previous OCTO longitudinal study, we identified an immune risk phenotype (IRP) of high CD8 and low CD4 numbers and poor proliferative response. We also demonstrated that cognitive impairment constitutes a major predictor of nonsurvival. In the present NONA longitudinal study, we simultaneously examine in a model of allostatic load IRP and compromised cognition in 4-year survival in a population-based sample (n = 138, 86–94 years). Immune system measurements consisted of determinations of T-cell subsets, plasma interleukin 6 and cytomegalovirus and Epstein–Barr virus serology. Interleukin 2 responsiveness to concanavalin A, using data from the previous OCTO (octogenarians) immune study, hereafter OCTO immune, was also examined. Cognitive status was rated using a battery of neuropsychological tests. Logistic regression indicated that the IRP and cognitive impairment together predicted 58% of observed deaths. IRP was associated with late differentiated CD8⁺CD28^–CD27^– cells (p <.001), decreased interleukin 2 responsiveness (p <.05) and persistent viral infection (p <.01). Cognitive impairment was associated with increased plasma interleukin 6 (p <.001). IRP individuals with cognitive impairment were all deceased at the follow-up, indicating an allostatic overload.

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