Search results

Responding to a question about this paper from a different thread. It does seem like if someone is sleep-deprived and thus falls asleep faster, one would expect to see impairments in sustained attention tasks. It might be too small a sample, and too much noise due to other causes of impaired...

Maybe you meant to post it in the other thread about ESS, and used the Insert Quote button on the wrong thread, since I see the quote in your post is from a different thread?

Here's one study: Plasma exchange therapy for the post COVID-19 condition: a phase II, double-blind, placebo-controlled, randomized trial (2025, Nature Communications) (Thread)

Good catch. That's very strange and misleading, especially when using the wrong number prominently in the abstract.

What's the reason for pointing this out about MSLT and ESS in this thread, as I only see the abstract describing using the psychomotor vigilance test (PVT) but not those other two? Did you mean to say that objective sleepiness (MSLT) and objective vigilance (PVT) don't reflect the same pathology?

Interesting! I've only read the the first paper so far, but it looks like what they have shown is basically that variants associated with complex traits (GWAS hits) and variants associated with changes in gene expression (eQTL hits) tend to be fundamentally different in several ways. They...

@Chris Ponting I think you might be interested in these other potentially overlapping loci, if you're not already aware of them. It seems like there might end up being a lot of genetic similarity between ME/CFS and pain.

Nice find! Just noting for the thread that this is the study that DecodeME said overlapped at CA10. They didn't look at the other loci because they weren't genome-wide significant. I wanted to compare the other loci, so I downloaded the summary stats for this study from GWAS Catalog, then did...

I think CACNA1E is the gene from DecodeME. Note also this other gene in the same family:

Any chance anyone knows the thread that the original image was discussed on?

The above explanation might have had some hard to understand parts, so I think it might be useful to describe TWAS with a really simple toy example. Hopefully, people can get a feel for what it is, in case we start seeing ME/CFS papers using it. To make it simple, I'll focus on one gene and one...

Now published: Genetic Insights into Circulating Complement Proteins in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Potential Inflammatory Subgroup Abstract Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-system illness with heterogeneity that...

I made a thread with some papers about TWAS: https://www.s4me.info/threads/a-gene-based-association-method-for-mapping-traits-using-reference-transcriptome-data-2015-gamazon-et-al.48810/

The aim of TWAS is to help identify the consequences of genetic variation in a GWAS on gene expression, which could help identify genes and tissues that may causally influence the disease. The basic steps of TWAS 1. First, a prediction model is created using data from large reference datasets...

The results reported from doing a transcriptome-wide association study (TWAS) based on depression GWAS data made me interested in learning more about TWAS. The abstract above is from the paper that introduced the first form of TWAS, PrediXcan. The first paper below introduced S-PrediXcan, a...

A gene-based association method for mapping traits using reference transcriptome data Abstract Genome-wide association studies (GWAS) have identified thousands of variants robustly associated with complex traits. However, the biological mechanisms underlying these associations are, in...

I agree with that last sentence that this seems to be a remarkable finding and supports the potential of GWAS and TWAS, because a decrease in dopamine receptors in the nucleus accumbens seems to be exactly what you would expect to be implicated in depression. DRD2 in nucleus accumbens was...

They looked for drugs that might target the depression-associated genes. It might be an interesting technique to use for ME/CFS genes. Discussion about some of these drugs:

Just copying the top enriched gene sets. It's basically synapse-related.

They talk about one area that might represent such a neuropsychiatric common component: Edit: 3p21 covers a wide area. Here's that range plotted with DecodeME data: A couple small spikes, but not significant.