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I made a thread for your paper, now that it's up: A Disequilibrium Oncotic Model of Brain Fluid Flux, 2026, Edwards

A Disequilibrium Oncotic Model of Brain Fluid Flux Edwards, Jonathan [Line break added] Abstract Application of the revised Starling model proposed by Levick and Michel (2010) suggests that cerebrospinal fluid (CSF) production is essential for maintenance of a low interstitial protein content...

If it was specifically the PVN, I think it'd be more interesting. But it seems like what you quoted is an AI mentioning PVN linking to NEGR1 because it's the area of interest that was asked about, while in reality NEGR1 may be involved everywhere in the brain. And if the question was about any...

Discussion after the above post regarding interferon and Dr. John Chia has been moved to the thread: John Chia - Clinician/Researcher

Ah, ok, so the idea is, if there are significant hits near a gene, plus significant hits near multiple enhancers or promoters which encourage expression of that gene, it might be more likely to be relevant. I just brushed up on the basics of what promoters and enhancers are with this video...

I haven't really been able to follow what exactly you're doing. Maybe you could lay out your overarching plan, and maybe describe what everything in one row of the table on this webpage means?

By my calculation, NEGR1 is a bit closer: Lead variant of the locus is at: chr1:73,126,414 NEGR1: chr1:71,395,943-72,282,539 LRRIQ3: chr1:74,026,015-74,198,187 Distance to NEGR1: 73126414 - 72282539 = 843875 Distance to LRRIQ3: 74026015 - 73126414 = 899601 Though the difference is so small...

I won't speak for others - maybe it would be good to focus in on those. I just like the nervous system angle based on the genetic evidence seeming to provide stronger evidence towards that (MAGMA from DecodeME and the model from Zhang 2025, to be clear).

Oh sorry, I did mischaracterize the quote I posted. I was thinking about this quote while writing that (which to be clear, seems like a somewhat reasonable idea to me):

But with regard to the idea of ME/CFS Science Blog quoted above, where if we suspect ME/CFS is a nervous system disease, and one of the nearest genes is a nervous system gene, then maybe it's worth giving it a little extra weight: [edit: see context below regarding the quote - I was thinking of...

Good question. To restate what's at issue here: if we have a significant locus, and we have no other information, what's the likelihood that the nearest protein-coding gene (NEGR1 in this case) is the pathogenic gene implicated by the significant variant? I realize I rather uncritically...

The lead variant of the locus looks to be close to the threshold (p = 1.19e-7). The locus doesn't overlap the gene, but that's the case for many DecodeME candidate genes.

That plot includes lots of non-coding RNA. This one shows NEGR1 and LRRIQ3 are the closest coding genes to this locus. NEGR1 is interesting because there seems to be growing evidence that it is relevant in depression and anxiety disorders, though it seems like the causal variant is different...

I'll need to read this paper thoroughly, but if I understood previous comments from @LizWorthey, the collection of variants presented is not based on trying to find variants that are found in multiple participants. Each individual was searched for variants indendently, and KCNJ18 turned out to...

Health Rising: 'Precision Medicine Required For ME/CFS? A Deep Genome Dive Uncovers Many Possible Causes'

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?