Relationship of systemic inflammation and cellular immunity with advancement of cognitive decline in patients with Alzheimer's disease

Abstract

AbstractObjectiveSystemic inflammation is known to be associated with Alzheimer's disease (AD) advancement. The aim of the present study was to examine the relationships of cognitive function in AD patients with the presence of systemic inflammation and immunological alterations.MethodsEight patients with AD and nine elderly individuals as a control group were enrolled, none of whom had a history of autoimmune diseases or were suffering from an infection. C‐reactive protein, interleukin‐6 and tumor necrosis factor‐α levels in serum were measured, while lymphocyte subsets were also determined using a flow cytometry system. In addition, two of the AD patients received repeated cognitive function and blood testing on an outpatient basis.ResultsIn the AD group, the percentages of CD3−CD16+CD56+ (natural killer) and CD4+CCR5+ (type 1 helper T) cells, and CD8+CD11a+ (cytotoxic T) lymphocytes were increased, whereas the percentages of CD19+ (B lymphocytes) and CD4+CD25brightCD127dim (regulatory T) cells were decreased as compared with the controls. Systemic inflammation, represented by elevated C‐reactive protein and interleukin‐6, was shown to aggravate cognitive function in both patients who underwent follow‐up outpatient examinations. However, lymphocyte subsets did not change in parallel with cognitive function.ConclusionsInflammatory acute clinical events have the potential to reduce cognitive function in AD patients, which could be partially attributed to a decrease in regulatory T cells in the blood. Furthermore, increased numbers of natural killer cells, cytotoxic T lymphocytes and type 1 helper T cells in these patients might reflect the presence of chronic inflammation, thus forming an immunological background.