Dementia

Inflammation May Predict Future Cognitive Decline

Systemic inflammation may contribute to the development of neurodegenerative diseases, according to the findings of a recent study.

In their study, the researchers assessed the plasma levels of systemic inflammatory markers of 1633 participants who were involved in the Atherosclerosis Risk in Communities Study. The mean age of participants was 53 years, 60% were women, and 27% were African American. Inflammatory markers used in the study included fibrinogen, albumin, white blood cell count, von Willebrand factor, and Factor VIII, which were combined to create an inflammation composite score for each participant. Episodic memory and regional brain volumes were assessed 24 years later and compared with circulating midlife inflammatory markers.
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Overall, the researchers found that every standard deviation in midlife inflammation composite score was associated with a 1788 mm3 greater ventricular, 110 mm3 smaller hippocampal, 519 mm3 smaller occipital, and 532 mm3 smaller Alzheimer disease signature region volumes, and reduced episodic memory 24 years later.

Participants with elevations of 3 or more inflammatory markers had, on average, 5% smaller hippocampal and Alzheimer disease signature region volumes compared with those with no midlife inflammatory marker elevations.

In addition, the researchers found that the association between midlife inflammation and late-life brain volume was modified by age and race. Younger and white participants with higher midlife systemic inflammation levels were found to have reduced brain volumes in later life.

“Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging,” the researchers concluded.

—Melissa Weiss

Reference:

Walker KA, Hoogeveen RC, Folsom AR, et al. Midlife systemic inflammatory markers are associated with late-life brain volume: the ARIC study [published online before print November 1, 2017]. Neurology. http:/​/​dx.​doi.​org/​10.​1212/​WNL.​0000000000004688.