In the field of peripheral nerve disorders and mostly immune-mediated peripheral nerve disorders, it’s sometimes difficult to monitor the activity of the disease. So sometimes the patients feel they feel weaker, but maybe the clinical examination that is the tool that we have today to monitor disease activity don’t see any change at all. So our examination is not sensitive enough sometimes...
In the field of peripheral nerve disorders and mostly immune-mediated peripheral nerve disorders, it’s sometimes difficult to monitor the activity of the disease. So sometimes the patients feel they feel weaker, but maybe the clinical examination that is the tool that we have today to monitor disease activity don’t see any change at all. So our examination is not sensitive enough sometimes. So we need biomarkers to monitor disease activity in this group of diseases. So our aim was to explore Guillain-Barre syndrome as a paradigmatic example of immune-mediated peripheral nerve disorder because it’s very aggressive, it’s very acute, and it’s monophasic, meaning that it occurs once and after several weeks it stops, disease activity stopped. So we can see the changes in disease activity from the acute phase to later in the disease. So it’s a good example in order to study proteomics in our case or biomarkers and then extrapolate it to other immune-mediated diseases. So that’s our aim, to see if there is something in the blood of patients with Guillain-Barre syndrome that could mark disease activity and help us in monitoring Guillain-Barre and other diseases and diagnosing as well. So what we did was to analyze more than 6,000 different proteins in samples from patients of Guillain-Barre syndrome. And we had samples from the acute phase before treatment was started, when the patients were in the hospital, and then after one year when patients were recovering. And we compared those to see if there were differences. And also we compared those with healthy controls. And yeah, like we, as I said, we analyzed more than 6,000 different proteins, and we saw that there were some proteins that were different from the acute phase to after one year in the same patient, and also compared to healthy controls. And we saw that these proteins were related to inflammation and lymphocyte activation. That was something that we kind of expected because it’s an inflammatory disease or an immune-mediated disease. And also we could see that in one year, patients had overexpression of proteins related to nerve regeneration and axonal guidance which also makes sense as these patients are recovering and the nerve is growing back or that’s what we were expecting. Moreover some of these findings we tried to validate it with other studies with other lab techniques because what we do what we used is SOMA scan which is an aptamer-based proteomic platform but this is very limited and for research So we needed something that we could implement in the clinical practice or in our lab. And we used two techniques actually, Meso Scale first and then ELISA, to try to validate these differences that we could see in some proteins, if we could see it also with these other techniques. And we actually did. We actually could. Like with ELISA, we could see that patients in the acute phase had higher values of… Actually we were studying mostly a candidate protein called serum amyloid A1, which is a protein related to inflammation and we saw that this protein was higher in the acute phase compared to at one year and compared to healthy controls and we could detect this with ELISA, not just with the SOMA scan. We are now trying to validate this with more controlled population with other neuromuscular diseases and other inflammatory diseases because this is, as I said, an inflammatory or a protein related to inflammation so we are not sure if it’s because of Guillain-Barré syndrome or if it’s because of an infection that most of the times occurs prior to Guillain-Barre. So we need to validate this with other post-infectious diseases to see if there are differences, or we’re just seeing the previous infection with this marker. But yeah, our idea is to try to validate this and other biomarkers that we have found, first in Guillain-Barre syndrome, and then try to extrapolate these findings to other immune-mediated neuropathies, mostly CIDP, and see if some of these markers could help us identify disease activity in relapses, or even if it could help us to prognosticate these patients to see the risk they have of a new relapse, or in the case of Guillain-Barré syndrome, have a bad prognosis. But we still we’re still doing this.
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