Is cognitive impairment (fibro fog) a result of pro-inflammatory cytokine excess?
Science: Memory impairment in mice was found to result from excess inflammatory cytokines, especially IL-6.
Conclusion: Fibro fog may be the result of inflammatory cytokine excess, especially IL-6 excess.
Inflammatory cytokines impair memory and learning: Fibro fog.
Cytokines are inter-cellular chemical messengers produced mostly by white blood cells.
Some are generally pro-inflammatory (inflammatory cytokines turn inflammation ‘on’) while others are generally anti-inflammatory (they turn inflammation ‘off’.)
Inflammatory cytokines, which are often elevated during sickness, are believed responsible for many of the common symptoms of illness and injury. That is, symptoms like sleepiness, fatigue, and mild ‘depression’ (collectively referred to as ‘sickness syndrome’) are observed in viral illness, bacterial infection, or during recovery from injury – because each of those conditions is associated with an increase in pro-inflammatory cytokines.
Not surprisingly, those who are sick do not remember or learn as well as those who are not sick. But it seems that’s not just because the other symptoms of illness get in the way of learning. Researchers have found that inflammatory cytokines directly affect the brain’s ability to process and retain information.
So the publication summarized below begins with the observation that pro-inflammatory cytokines inhibit learning and memory. That’s a given – but what these researchers hoped to discover was the contribution made by a specific inflammatory cytokine, IL-6, to problems with learning and memory.
First, each group of mice was taught how to run through a maze to find a piece of cheese. Both groups did just fine – the mice quickly learned how to navigate the maze.
Each group was then injected with an agent that caused inflammation. That of course led to an increase in pro-inflammatory cytokine IL-6 in the normal mice – but not in mice with the genetic defect. Note that the genetic defect mice still had inflammation. They were still sick little mice – they just didn’t have IL-6 excess.
What happens? The normal (but sick) mice have a really hard time running the maze. But the sick mice without IL-6 still run the maze nearly as well as before they were made ill.
Likewise, the sick mice without IL-6 can still learn to run a new maze, whereas the others can’t.
So it seems IL-6 excess leads to difficulties with memory and learning – at least in mice – and probably in humans as well.
What does all this have to do with fibromyalgia?
Perhaps quite a bit.
We know fibromyalgia is not an inflammatory condition – at least not in the typical sense. But a lot of research shows that inflammatory cytokines are elevated – sometimes dramatically – in those with fibromyalgia. In fact IL-6 is often markedly elevated in those with fibromyalgia.
We suspect IL-6 elevation is the cause of fibro fog.
Of interest, IL-6 has also been shown to be elevated in other conditions, such as lupus, that are also associated with impaired memory and learning. It looks like IL-6 causes fog wherever it goes – mice, humans, fibromyalgia, lupus.
Interleukin-6 facilitates lipopolysaccharide-induced disruption in working memory and expression of other proinflammatory cytokines in hippocampal neuronal cell layers.
Summary of the Abstract
Pro-inflammatory cytokines inhibit learning and memory but the significance of IL-6 in acute cognitive deficits is not known.
Regular Mice injected intraperitoneally with lipopolysaccharide exhibited deficits in working memory. However, those mice unable to produce IL-6 experienced no deficit in memory following the same injection.