APOE ϵ4 modifies the relationship between infectious burden and poor cognition
Chen Zhao1, Kevin Strobino1, Yeseon Park Moon1
1Department of Neurology (C.Z., K.S., Y.P.M.), Vagelos College of Physicians and Surgeons, Columbia University, New York, NY; Department of Neurology (C.Z.), Penn State Health Milton S. Hershey Medical Center; Department of Public Health Sciences (C.Z.), Pennsylvania State College of Medicine, Pennsylvania State University, Hershey, PA; Department of Biostatistics (Y.K.C.), Mailman School of Public Health, Columbia University, New York, NY; Departments of Neurology (R.L.S.), Public Health Sciences, and Human Genomics, Miller School of Medicine, University of Miami, Miami, FL; Cognitive Neuroscience Division (Y.S.), Department of Neurology, Vagelos College of Physicians and Surgeons, Taub Institute for Research of Alzheimer's Disease and the Aging Brain, Gertrude H. Sergievsky Center, Columbia University, New York, NY; Department of Neurology (M.S.V.E.), Vagelos College of Physicians and Surgeons; and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York, NY.
Objective:
We investigated whether APOE ϵ4 is an effect modifier of the association between infectious burden (IB) and poor cognition in a multiethnic cohort, the Northern Manhattan Study.
Methods:
IB was assessed by a quantitative weighted index of exposure to common pathogens associated with vascular risk, infectious burden index (IBI), and by serology for individual infections. Cognition was assessed by completion of the Mini-Mental State Examination at baseline and a full neuropsychological test battery after a median follow-up of approximately 6 years. Adjusted linear and logistic regressions estimated the association between IBI and cognition, with a term included for the interaction between APOE ϵ4 and IBI.
Results:
Among those with full neuropsychological test results (n = 569), there were interactions between IBI and APOE ϵ4 (p = 0.07) and herpes simplex virus 1 (HSV-1) and APOE ϵ4 (p = 0.02) for processing speed. IBI was associated with slower processing speed among non-ϵ4 carriers (β = -0.08 per SD change in IBI, 95% confidence interval [CI] -0.16 to -0.01), but not among APOE ϵ4 carriers (β = 0.06 per SD change in IBI, 95% CI -0.08 to 0.19). HSV-1 positivity was associated with slower processing speed among non-ϵ4 carriers (β = -0.24, 95% CI -0.45 to -0.03), but not among APOE ϵ4 carriers (β = 0.27, 95% CI -0.09 to 0.64).
Conclusions:
Potential effect modification by the APOE ϵ4 allele on the relationship of infection, and particularly viral infection, to cognitive processing speed warrants further investigation.
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