Christopher A. Baker

Firstgen in Yale Center for Infection & Immunity using imaging technologies to study pain in long COVID and similar syndromes.

[Christopher A. Baker @bakermind]

A new study co-led by Yale scientists reveals that antibodies from some long COVID patients attacked brain and nerve tissues, a finding that could point toward treatments.
https://t.co/kmkn1Kj2TF

[Christopher A. Baker @bakermind]

@BrandonWarmke I believe some faculty have had those ideas but have learned that it's kind of illegal. It would also create a system in which senior faculty pay students more than junior faculty, which is not good for the department

[Christopher A. Baker @bakermind]

@michaelzlin Not sure that's why Anthropic has that value. It's that the tech theoretically allows every institution to eliminate a lot of entry level analyst labor cost and increase productivity. And many have FOMO on the big boom. It's massive hype but not completely unfounded

[Christopher A. Baker @bakermind]

I was interested until I saw it was in Nature Scientific Reports. That journal's slop status is becoming legendary

[Harry Spoelstra @HarrySpoelstra]

Long-COVID: Ultrasensitive multiplex protein biomarker profiling reveals subclinical neuroinflammatory and innate immune dysregulation without correlation to symptom severity

🚨LongC0VID patients show a hidden cytokine-storm + neuroinflammation signature that only ULTRA-SENSITIVE PROTEOMICS can detect. Yet the biology doesn’t match how sick they feel. The real driver may be central sensitisation or brain rewiring.🤔

➡️Very interesting small Norwegian study, bear with me!

- Routine labs are normal in longC0VID, yet patients have persistent fatigue, cognitive issues, depression, and other symptoms more than a year after infection.

- In this matched case-control study (48 longC0VID patients vs 48 fully recovered controls, median ~65–72 weeks post-infection), ultrasensitive NULISAseq proteomics (123 CNS/immune biomarkers at attomolar sensitivity) detected clear biological differences invisible to standard tests.

- 19 proteins were significantly dysregulated; top upregulated markers included CCL22, IL-6R and CST3. Pathway analysis showed activated Pathogen-Induced Cytokine Storm, Neuroinflammation, and IL-10 signalling pathways, pointing to low-grade innate immune activation and neuroinflammatory signals.

- Hierarchical clustering split longC0VID patients into two biological subgroups (one dominated by metabolic reprogramming/mitochondrial dysfunction and cytokine-storm features, the other by neuroinflammation and related signalling).

- Critically, neither the protein levels nor the biological clusters correlated with symptom severity, fatigue, depression, cognitive scores, or any patient-reported outcomes. Conventional PCA also showed no clear patient-control separation.

- The study does not examine reinfection or vaccination status. It simply compares people with ongoing longC0VID symptoms versus people who fully recovered, both more than one year after documented SARSCoV2 infection.

➡️The authors conclude that subclinical immune/neuroinflammatory dysregulation is present but does not map directly onto how sick patients feel, implying additional mechanisms (central sensitisation, epigenetic changes or similar) convert peripheral signals into the clinical picture.

‼️So, according to these authors, LongC0VID harbours a real but hidden biological footprint of innate immune activation and neuroinflammation that standard medicine cannot see and that does not match the intensity of patients’ symptoms, pointing to brain-level amplification mechanisms as the missing link.

‼️Important take-away:
1. For the millions still living with longC0VID, this matters because it shows why ordinary blood tests are repeatedly “normal” while people remain disabled. It validates that low-level immune and neuroinflammatory changes can persist >1 year and explains the frustrating mismatch between lab results and lived experience. Clinically it argues against relying solely on symptom scores or standard inflammatory markers for diagnosis or trial endpoints, and it supports research into treatments that address both residual immune signalling and central sensitisation/pain-processing pathways. It also reinforces that longC0VID is heterogeneous at the molecular level even when symptoms look similar.
2. Finally, this study doesn’t contradict earlier ultrasensitive findings, actually, it confirms and extends them. The attomolar view of longC0VID as a state of low-grade, heterogeneous innate immune and neuroinflammatory dysregulation that is largely invisible to routine labs and poorly linked to symptom intensity is holding up across platforms and other cohorts.
We’re getting somewhere!
#AvoidSars2 #AvoidReinfection
https://t.co/5KTEsVgbk9

[Christopher A. Baker @bakermind]

@ZdenekVrozina Not "mice". "Mice engineered to have amyloid deposition". Your headline makes it sound like wild-type mice get amyloid from repeated infection. This is not a common mutation to be found in humans. I do think infection can exacerbate susceptibility but want to take care.

[Christopher A. Baker @bakermind]

@MaryBowdenMD You're a Miller fan?

[Christopher A. Baker @bakermind]

@silvirouskin Yeah that's why infectious disease is so rare in poverty areas 😐

[Christopher A. Baker @bakermind]

@drseanmullen If you think that pandemic ineptitude and pro-virus propaganda contributed to infections and therefore LC, it might not be so far off

[Christopher A. Baker @bakermind]

@SalvMattera It's been discussed but we should also think about mechanism. Casey is talking about autoantibody transfer, which happens in animals but shouldn't self sustain. Revival mentions actual viral transfer, but AFAIK viremia in LC is low to zero. OTOH persistent Ebola might transmit.

[Christopher A. Baker @bakermind]

@StevenSalzberg1 @SciReports @SpringerNature If you think $2800 is exorbitant, you should see the costs of making papers OA at other Nature journals

[Christopher A. Baker @bakermind]

@Isanthropia What use of the past tense? I guess you want him to say "has accelerated" instead of "was accelerated"? But if the data doesn't include 2026, "was" might be more appropriate; if aging increasED 2020-2024 we don't know if it has continued to increase since

[Christopher A. Baker @bakermind]

@MarcHvidkjaer This simply shows that being a professor at Harvard is lucrative. It's manipulative to show the data in a line graph, which implies that the same people are progressing from Harvard grad to Harvard faculty. Some highly paid Harvard faculty didn't get their PhDs from Ivy League

[Christopher A. Baker @bakermind]

@fperrywilson Why would anyone want to model votes as random probabilities? It's allegedly NOT random, but a product of choice. The real test would be if the distribution changes were not continuous but instead more discrete

[Christopher A. Baker @bakermind]

@libsoftiktok Congrats. You've discovered that voting is not a random event. That's why we don't choose our representatives by a coin toss

[Christopher A. Baker @bakermind]

@SalvMattera A virus' interests are just to replicate. I have yet to read the paper, but it seems to suggest increased epigenetic clock rates post SARS-COV-2 incidence. Seems hard to assign such changes solely to the pandemic; I'm more interested in the same comparisons in LC vs non-LC

[Christopher A. Baker @bakermind]

@ClownWorld One says Republican
One says Other
And the incumbent has an asterisk.
I wouldn't be surprised if 3600 people meant to say "none of the above"

[Christopher A. Baker @bakermind]

@RepNancyMace OK no one is making you do that, but why do you refer to yourself with plural pronouns

[Christopher A. Baker @bakermind]

@mecfsskeptic I didn't sign up for the blog so I can't read the statement. Suffice it to say that problematic design is always a red flag but I don't think that means that 1) "long COVID" doesn't exist, or 2) there are zero long-term consequences of acute infections

[Christopher A. Baker @bakermind]

@1goodtern I did think about writing a grant to examine epigenetic clocks in long COVID versus everyone else; maybe we should bring that back to the front burner, @EricTopol ?

[Christopher A. Baker @bakermind]

@Rayleigh_com @tylerblack32 Even without a college degree, they are still smart enough to recognize they'd been duped