Plasma proteomics show altered inflammatory and mitochondrial proteins in patients with ... post-acute sequelae of SARS-CoV-2, 2023, B. Hanson et al

The Hanson in the author list is Barbara Hanson of North-Western University, Chicago.
@DMissa, one in your wheelhouse.

From the posted excerpts, it looks interesting. The separations aren't perfect, but I guess there could be quite a bit of daily variation in the levels of the proteins depending on activity levels and other things, even in the healthy people.

 

Just worth noting this clinic, may be of interest to people with Long covid. They are doing studies and seem to have people assessed by specialists, so even with just that, they are well ahead of many clinics. They don't appear to assess for PEM though.

And also noting the NIH Toolbox for assessing cognitive function.

This is the method for identifying specific proteins. There's a normalising process.

So, some differences in age between the people who had had Covid (both with and without persisting symptoms) and the healthy controls. I had wondered about sex ratios, but they report these were similar. I guess one major difference between the NP (neuroPASC) and the other two groups might be activity levels, but, off the top of my head, I can't think why lower activity levels would cause an increase of mitochondrial proteins being expelled into the blood.

 

They found more depression and anxiety in the NeuroPASC cohort, but it's worth noting that these patients are being assessed 6 months into their illness, so they won't have had time to adapt and come to terms with the abrupt negative change in their lives.

So, attention was the most affected cognitive measure. Interesting that processing speed wasn't significantly different. I'm not quite sure what they mean by that last sentence and haven't bothered to understand it; perhaps the fluctuating nature of cognitive impairment in people with mild PASC is relevant. Figure 2b gives the data, so you can draw your own conclusions. The 50% line is the population average given the individual's age (and maybe other things).


According to Fig 2A and 2C, only 34 of the NeuroPASC patients reported their subjective cognition, and only 35 patients reported their subjective fatigue. So, these samples are quite a lot lower than the 46 cohort size that is reported. That raises questions about the demographic characteristics of these smaller samples. Why were these patients surveyed while other patients in the 46 were not? The smaller samples becomes important when it comes the Figures 3A and 3B

To understand this, we need to understand what is being compared. For example, Figure 3A is, if I'm understanding it right, making comparisons within the 34 NeuroPASC patients. So, from Table 2c, we know that 2/3 of patients reported cognitive problems that were 1 SD worse than the normalised population average, and so something like 22 patients are in the group described as 'experiencing brain fog' and around 12 were not experiencing brain fog. So, figure 3A compares the proteins in the brain fogged NeuroPASC people with the un-brain fogged Neurological PASC people. That's all very well, but I don't think it's really the comparison we want.

I think it would have been better to compare the proteins in the subset of the NeuroPASC with cognitive dysfunction, or fatigue (and PEM would have been good too) against the healthy controls and the convalescent controls. I think the comparisons within the NeuroPASC group start to get too small, and there are the inaccuracies in measuring subjective symptoms like fatigue (e.g. people still trying to do their usual activities will report more fatigue than people who have given up work).

So, I'm inclined to not pay much attention to Figures 3A and 3B.

(I've got to take a break, but I don't want to leave things suggesting I'm dismissing the whole study. The Cox7A1 finding sounds interesting, and Figure 3c looks convincing, so I do want to poke into it some more.)