Abstract
Serum pro‐inflammatory markers may contribute to dementia pathophysiology and cognitive impairment. In a population‐representative birth cohort, serum C‐reactive protein (CRP), interleukin‐6 (IL‐6), and white cell count (WCC) were measured at age 60‐64 years and cognition was assessed using the Addenbrooke's Cognitive Examination (ACE‐III) at age 69 years. Higher baseline CRP and IL‐6 were associated with lower ACE‐III scores, but associations were attenuated on adjustment for educational attainment, sex, and other modifiable life course factors. No associations were found for CRP, IL‐6, and WCC with visual search speed or verbal memory. In conclusion, the relationship between increased baseline systemic inflammation and poorer cognition in later life may be explained by, or share pathways with, education and other modifiable life course factors.
Highlights
Neuroinflammation is a feature of Alzheimer’s disease,[1] the degree to which pathophysiology may be driven by systemic inflammation is unclear
We investigated this in a birth cohort with the advantage of accurate ascertainments of exposures across the whole life course, along with detailed assessment of cognition, to answer the following questions: 1. Is systemic inflammation prospectively associated with later cognitive impairment?
Our findings demonstrated that associations between mid-life baseline IL-6 and C-reactive protein (CRP) with later life cognitive impairment were explained by educational attainment and modifiable life course factors
Summary
Neuroinflammation is a feature of Alzheimer’s disease,[1] the degree to which pathophysiology may be driven by systemic inflammation is unclear. Systemic illnesses with a pro-inflammatory response may contribute to neurodegeneration and worsening dementia severity.[2,3,4,5] findings from epidemiological studies have been inconsistent[6,7,8,9,10,11]; discrepancies may in part reflect complexities in modelling the temporal patterns of modifiable life course factors on both systemic inflammation and cognition These factors include educational attainment,[12] body mass index (BMI),[13] alcohol intake,[14] smoking, and exercise.[15] Many of these exposures are time-varying and so apparent associations with inflammation and cognition may be subject to reverse causation. Is any association explained by modifiable lifestyle risk factors, such as early life educational attainment, body mass index, midlife exercise, alcohol consumption, or smoking?
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