AGE

, Volume 34, Issue 5, pp 1295–1308

The association between systemic inflammation and cognitive performance in the elderly: the Sydney Memory and Ageing Study

  • Julian N. Trollor
  • Evelyn Smith
  • Emmeline Agars
  • Stacey A. Kuan
  • Bernhard T. Baune
  • Lesley Campbell
  • Katherine Samaras
  • John Crawford
  • Ora Lux
  • Nicole A. Kochan
  • Henry Brodaty
  • Perminder Sachdev
Article

DOI: 10.1007/s11357-011-9301-x

Cite this article as:
Trollor, J.N., Smith, E., Agars, E. et al. AGE (2012) 34: 1295. doi:10.1007/s11357-011-9301-x

Abstract

Inflammation may contribute to cognitive decline and dementia. This study examined the cross-sectional relationships between markers of systemic inflammation (C-reactive protein, interleukins-1β, -6, -8, -10, -12, plasminogen activator inhibitor, serum amyloid A, tumour necrosis factor-α and vascular adhesion molecule-1) and cognitive function in 873 non-demented community-dwelling elderly participants aged 70–90 years. Regression analyses were performed to determine the relationships between cognitive domains and inflammatory markers, controlling for age, sex, education, cardiovascular risk factors, obesity and other metabolic factors, smoking, alcohol consumption, depression and presence of the apolipoprotein ε4 genotype. Regression analyses were repeated using four factors derived from a factor analysis of the cognitive tests. After Bonferroni correction for multiple testing, associations remained between raised levels of interleukin-12 and reduced performance in processing speed. Marked sex differences were noted in the abovementioned findings, with only females being significantly affected. Using the four factors derived from the factor analyses of cognitive test as dependent variables, interleukins-12 and -6 were both associated with the processing speed/executive function factor, even after controlling for relevant confounding factors. Thus, markers of systemic inflammation are related to cognitive deficits in a non-clinical community-dwelling elderly population, independent of depression, cardiovascular or metabolic risk factors, or presence of apolipoprotein ε4 genotype. Additional research is required to elucidate the pathophysiology and longitudinal development of these relationships.

Keywords

InflammationAgeingCytokinesInflammagingCognitionDementia

Copyright information

© American Aging Association 2011

Authors and Affiliations

  • Julian N. Trollor
    • 1
    • 4
  • Evelyn Smith
    • 1
    • 4
  • Emmeline Agars
    • 1
  • Stacey A. Kuan
    • 8
  • Bernhard T. Baune
    • 9
  • Lesley Campbell
    • 6
    • 7
  • Katherine Samaras
    • 6
    • 7
  • John Crawford
    • 4
  • Ora Lux
    • 2
    • 3
    • 4
  • Nicole A. Kochan
    • 2
    • 4
  • Henry Brodaty
    • 4
    • 5
  • Perminder Sachdev
    • 2
    • 4
  1. 1.Department of Developmental Disability Neuropsychiatry, School of PsychiatryUniversity of New South WalesSydneyAustralia
  2. 2.Neuropsychiatric InstitutePrince of Wales HospitalRandwickAustralia
  3. 3.South-Eastern Area Laboratory ServicesPrince of Wales HospitalRandwickAustralia
  4. 4.Brain and Aging Research Program, School of PsychiatryUniversity of New South WalesSydneyAustralia
  5. 5.Dementia Collaborative Research Centre, School of PsychiatryUniversity of New South WalesSydneyAustralia
  6. 6.Garvan Institute of Medical ResearchDarlinghurstAustralia
  7. 7.Department of EndocrinologySt Vincent’s HospitalDarlinghurstAustralia
  8. 8.The Benevolent SocietyPaddingtonAustralia
  9. 9.Discipline of Psychiatry, School of MedicineUniversity of AdelaideAdelaideAustralia