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Dysregulation of brain and choroid plexus cell types in severe COVID-19, Yang et al., 2021, Nature

Discussion in 'Epidemics (including Covid-19, not Long Covid)' started by Ron, Jun 25, 2021.

  1. Ron

    Ron Established Member (Voting Rights)

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    Abstract in second post

    https://abc7news.com/health/stanford-researchers-may-have-answer-to-treat-covid-brain-fog/10828320/

    Working with a team in Germany, they found that the virus triggers brain inflammation, which leads to symptoms similar to Alzheimer's and Parkinson's.


    "Researchers at Stanford Medicine collaborated with counterparts at Germany's Saarland University. An analysis of brain tissue from eight patients showed inflammation that creates brain fog or cognitive decline, similar to symptoms of Alzheimer's and Parkinson's."

    "I think it will be interesting and important to figure out whether this inflammation could actually be targeted or treated and where the inflammatory, anti-inflammatory treatments could help alleviate some of these symptoms," said Prof. Tony Wyss-Coray PhD, whose lab had 20 researchers engaged in the project.
     
    Last edited by a moderator: Jun 25, 2021
    Yessica, Lisa108, sebaaa and 8 others like this.
  2. Jaybee00

    Jaybee00 Senior Member (Voting Rights)

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    https://www.nature.com/articles/s41586-021-03710-0

    Posted by @rvallee in COVID thread but deserves its own thread.

    Published in Nature

    Abstract
    Though SARS-CoV-2 primarily targets the respiratory system, patients and survivors can suffer neurological symptoms1–3. Yet, an unbiased understanding of the cellular and molecular processes affected in the brains of COVID-19 patients is still missing. Here, we profile 65,309 single-nucleus transcriptomes from 30 frontal cortex and choroid plexus samples across 14 control (including 1 terminal influenza) and 8 COVID-19 patients. While a systematic analysis yields no molecular traces of SARS-CoV-2 in the brain, we observe broad cellular perturbations which predict that choroid plexus barrier cells sense and relay peripheral inflammation into the brain and show that peripheral T cells infiltrate the parenchyma. We discover COVID-19 disease-associated microglia and astrocyte subpopulations that share features with pathological cell states reported in human neurodegenerative disease4–6. Synaptic signaling of upper-layer excitatory neurons—evolutionarily expanded in humans7 and linked to cognitive function8—are preferentially affected in COVID-19. Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression. Our findings and public dataset provide a molecular framework to understand COVID-19 related neurological disease observed now and which may emerge later.

    Stanford researchers may have answer to why COVID patients develop 'brain fog'
    https://abc7news.com/health/stanford-researchers-may-have-answer-to-treat-covid-brain-fog/10828320/

    Brain inflammation in COVID-19 cases looks eerily similar to Alzheimer’s disease
    https://www.studyfinds.org/brain-inflammation-covid-alzheimers/


     
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  3. Jaybee00

    Jaybee00 Senior Member (Voting Rights)

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    oops also posted below now. Not very cheerful about the results of this study.
     
  4. MeSci

    MeSci Senior Member (Voting Rights)

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  5. Peter Trewhitt

    Peter Trewhitt Senior Member (Voting Rights)

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    I suppose we need to answer the question are the cognitive issues in such as Alzheimer’s the result in part of the disease process that causes the death of brain cells, perhaps inflammation, as well as the loss of brain cells itself, or just the result of the loss of brain cells alone. In Parkinson’s my knowledge is so very out of date, given improvements in drug treatment, do we know how much of Parkinson’s related dementia is currently a result of Parkinson’s or how much it continues to be caused by the long term use of the drugs treating the Parkinson’s? Going back forty or fifty years when my grandmother had Parkinson’s an dementia and when I was an undergraduate, long term use of the then Parkinson’s medication was a major contributory factor.

    What surprises me is the jump to Alzheimer’s and Parkinson’s, when at least in relation to the variation we see in say ME, multiple sclerosis might be superficially a more obvious comparator.

    Comparison between Long Covid and ME and these neurodegenerative conditions does raise this issue as why for most their brain fog is not an ongoing deterioration or that recovery or at least significant improvement is a regular occurrence with the resolution of PEM, until the next episode of PEM or until the next relapse.

    Never the less the finding of neuro-inflammation in Covid is a big step forward. I for one would jump at a treatment for brain fog.
     
  6. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    This looks like meaningless hype to me. Why don't they give us some meaningful background to the cases? Since when were single nucleus transcriptomes useful in this sort of situation and so on. This looks like a group of people with very expensive equipment who have no idea what the results of using it mean.

    Maybe the patients had hypoxia with secondary coagulapathy and ischaemic damage. Something as simple as that would cover what is in the abstract.
     
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  7. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    I don't think that is realistic. People die from Covid regularly, and often from hypoxia. Hypoxia will lead to brain ischaemia with an inflammatory reaction. The finding seem to me too banal to even bother with.

    Researchers seem to have completely lost their bearings in terms of basic background understanding of pathology. I cannot see the point of doing transciptomes on cells from people whose brains are shot from the effect of pneumonia.
     
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  8. Peter Trewhitt

    Peter Trewhitt Senior Member (Voting Rights)

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    Thank you @Jonathan Edwards for pointing this out. I had assumed that they had identified neuro inflammation in Long Covid rather than thinking through that the autopsies were of people dying at the acute stage, who had they lived may or may not have gone on to develop long Covid.
     
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  9. glennthefrog

    glennthefrog Established Member (Voting Rights)

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    this is relevant to me. I've had ME for 23 years and got covid19 last October. Covid reactivated a symptom that I haven't had in a while, an "internal itch" limited only and precisely to the whole left side of my body, it was one of the first symptoms I experienced when I developed ME 23 years ago and with covid, it reappeared with an extremely increased intensity, to the point of not letting me sleep at night. I believe the virus infected my brain, interacting with a previous anomaly related to my ME or whatever ME related disease that caused said symptom to appear 23 years ago (I suspect a virus, the one that triggered ME in the first place). An interisting note, in 23 years I never had the chance to try any treatment against that itch, as 23 years ago I didn't have access to any drugs... however, this time, I had OXICODONE, and I found that it improved the itching remarkably, what could this mean? does this mean that the itch shares, at a physiological level, the same causes as brain related pain? note it limits itself strictly to a single side of my body, from head to toes, pointing, I believe, to brain involvement. What do you think? did someone ever had this symptom? by the way, my brain SPECT scan and FUNCTIONAL MRI show clear abnormalities, it's obvious for me that there's something wrong with it
     
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  10. Jaybee00

    Jaybee00 Senior Member (Voting Rights)

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    If this paper is so flawed, I’m surprised *I guess* that it survived the severe peer review of Nature.
     

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