Ankylosing spondylitis patients may be at risk of developing dementia
19 Aug 2020
Ankylosing spondylitis (AS) appears to convey about a 20-percent increased risk of developing dementia, according to the results of a systematic review and meta-analysis.
Researchers pooled data from three retrospective cohort studies and one case-control study, which corresponded to a total population of 156,418 individuals. Two studies were conducted in Europe and the other two, in Asia. All of them were of good quality, with a Newcastle-Ottawa score of at least 7.
On random-effects analysis, the risk of incident dementia was significantly higher among patients with AS than among controls (relative risk, 1.19, 95 percent confidence interval, 1.01–1.41; I2, 76 percent).
The funnel plot was relatively symmetric and was not suggestive of presence of publication bias, although this should be interpreted in light of the studies included.
The researchers enumerated several potential explanations for the finding. First is the involvement of chronic inflammation generated by AS. Chronic inflammation may have a direct negative effect on the central nervous system, and there is evidence that elevated levels of several proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumour necrosis factor (TNF)-α, may induce neurodegeneration. [Cold Spring Harb Perspect Med 2012;2:a006346; J Cent Nerv Syst Dis 2017;9:1179573517709278]
Meanwhile, AS patients are often sedentary due to pain and limited back mobility. Physical inactivity contributes to an increased risk of cognitive decline and predisposes these patients to a higher risk of dementia. [Biomed Res Int 2017;2017:e9016924]
The third possible underlying mechanism relates to corticosteroids, which are used in certain cases for patients with significant peripheral joint involvement and those with uveitis, according to the researchers. Corticosteroids are said to play a role in the regulation of synaptic plasticity in the hippocampus, the core area for learning and memory. [Front Cell Neurosci 2012;6:12]