Affiliations: [a] VA San Diego Healthcare System, San Diego, CA, USA
| [b] Department of Psychiatry, University of California, La Jolla, CA, USA
| [c] Laboratory of Behavioral Neuroscience, National Institute on Aging, Baltimore, MD, USA
| [d] Department of Anatomy & Neurobiology and Neurology, Framingham Heart Study, Boston University School of Medicine, Boston, MA | [e] Department of Epidemiology, Boston University School of Public Health, Boston, MA | [f] Department of Epidemiology, Baltimore, MD, USA
| [g] Department of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
| [h]
Johns Hopkins Center on Aging and Health, Baltimore, MD, USA
Correspondence:
[*]
Correspondence to: Katherine Bangen, PhD, 9500 Gilman Drive, Mail Code 151B, San Diego, CA 92093-9151, USA.
Tel.: +1 858 552 8585/Ex5794; Fax: +1 858 642 6340; E-mail: kbangen@ucsd.edu.
Abstract: Metabolic syndrome (MetS) has been linked to increased risk of developing cognitive impairment and dementia including Alzheimer’s disease. It remains unclear whether and at what stage in the adult lifespan MetS and its components begin to alter the trajectory of cognitive performance. In the present study, 2,892 Framingham Offspring participants completed health assessments every four years since 1971 and underwent repeat neuropsychological testing from 1999 to 2014. We estimated the associations of levels and changes in cognitive trajectories with hazard of MetS using a joint growth/survival model. All models were adjusted for baseline age, sex, education, and smoking status. Findings showed that both mid-life and late-life MetS were associated with lower level of cognitive functioning but not cognitive trajectories. Associations were strongest among those who were nondemented and apolipoprotein (APOE) ɛ4 noncarriers. In addition, individuals with the most rapid cognitive decline were more likely to have MetS. The pattern of results showed that associations between MetS and cognition varied, depending upon whether the sample was stratified by genetic and cognitive status and whether we considered cognitive performance as a continuous variable or examined categorical groupings. Given that mid-life MetS was associated with poorer cognition at age 55, cognitive changes may occur early during the MetS process. Our findings suggest that those with MetS are at greater risk of dementia given their lower level of cognitive functioning and also suggest that MetS may be a risk factor for decline in the absence of known risk factors including the APOE ɛ4 allele.
