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Source: Long COVID - NEUROCOVID  Jan 11, 2022  2 years, 1 month, 2 weeks, 3 days, 16 hours, 27 minutes ago

More Great News! Stanford-Yale Study Shows Even Mild SARS-CoV-2 Infection Can Cause Multi-Lineage Cellular Dysregulation And Myelin Loss In The Brain!

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More Great News! Stanford-Yale Study Shows Even Mild SARS-CoV-2 Infection Can Cause Multi-Lineage Cellular Dysregulation And Myelin Loss In The Brain!
Source: Long COVID - NEUROCOVID  Jan 11, 2022  2 years, 1 month, 2 weeks, 3 days, 16 hours, 27 minutes ago
It’s really getting to be a mentally orgasmic day as we are rejoicing about more emerging studies showing both the short term and long-term health damages that SARS-CoV-2 infections can cause. With more than 310.5 million people infected as of today from the SARS-CoV-2 infections according to official figures. (In reality, even the WHO and U.S. CDC has admitted that the true figures could be anything from 3 to 6 fold!) plus with Omicron sweeping across large populations and infecting anyone in its way, it is great that a large population of the world is going to suffer the consequences of long COVID with a substantial percentage going to be ending up with fatal outcomes eventually and most of these morons are not even going to be aware of what is happening to them!

Though the number of COVID-19 deaths so far is a bit disappointing ie only 5.498 million as of today, we can be rest assured that excess deaths will keep on rising and make up for these shortfalls and hopefully the next few surges with new variants emerging in coming months will make up for these low figures especially once ADE, original antigenic sin, immune printing and viral priming comes into play more significantly. (We prepared 10 boxes for the COVID-19 death figures but disappointingly we are only stuck at the 7th box for such a long time, just can’t wait till the figures start rising and all the boxes start getting filled…forget about compassion and religion, the last two years has thought us that most people are hypocrites, judgmental, pathetic and fake!...we are not the least perfect but imagine when you discover that hypocrites judging you are far worse and yet they talk about others going to hell!)
I personally cannot wait for all these stupid morons and their loved ones that keep on saying that Omicron is mild and there is no need for stringent measures or panic etc and even those ignorant twats saying that COVID is going to be endemic. (You guys are going to really laugh…garbage Thai media reported today that even certain ignorant stupid health authorities can actually make the COVID situation turn into an endemic scenario!! will be amazed how stupid most Thai doctors actually are!)
Back to study, researchers from Stanford University, Yale University, U.S.National Institute of Neurological Disorders and Stroke, Mount Sinai School of Medicine, U.S. National Cancer Institute, University of Iowa, , Uniformed Services University of Health Sciences, Office of Chief Medical Examiner-New York and Howard Hughes Medical Institute have in a new study found that even mild SARS-CoV-2 infection can cause multi-lineage cellular dysregulation and myelin loss in the brain!
It has already been known and also proved in many recent studies that survivors of SARS-CoV-2 infection frequently experience lingering neurological symptoms, including impairment in attention, concentration, speed of information processing and memory.
Interestingly this long-COVID cognitive syndrome shares many features with the syndrome of cancer therapy-related cognitive impairment (CRCI).
Neuroinflammation, particularly microglial reactivity and consequent dysregulation of hippocampal neurogenesis and oligodendrocyte lineage cells, is central to CRCI.
The study team hypothesized that similar cellular mechanisms may contribute to the persistent neurological symptoms associated with even mild SARS-CoV-2 respiratory infection.
The study team explored neuroinflammation caused by mild respiratory SARS-CoV-2 infection, without neuroinvasion, and effects on hippocampal neurogenesis and the oligodendroglial lineage.
Utilizing a mouse model of mild respiratory SARS-CoV-2 infection induced by intranasal SARS-CoV-2 delivery, the study team alarmingly found white matter-selective microglial reactivity, a pattern observed in CRCI.
Interestingly human brain tissue from 9 individuals with SARS-CoV-2 infection exhibited the same pattern of prominent white matter-selective microglial reactivity.
The study finding showed that in mice, pro-inflammatory CSF cytokines/chemokines were elevated for at least 7-weeks post-infection; among the chemokines demonstrating persistent elevation is CCL11, which is associated with impairments in neurogenesis and cognitive function.
Humans experiencing long-COVID with cognitive symptoms (48 subjects) similarly demonstrate elevated CCL11 levels compared to those with long-COVID who lack cognitive symptoms (15 subjects).
Impaired hippocampal neurogenesis, decreased oligodendrocytes and myelin loss in subcortical white matter were evident at 1 week, and persisted until at least 7 weeks, following mild respiratory SARS-CoV-2 infection in mice.
The study findings presented here illustrate striking similarities between neuropathophysiology after cancer therapy and after SARS-CoV-2 infection, and elucidate cellular deficits that may contribute to lasting neurological symptoms following even mild SARS-CoV-2 infection.
The study findings were published on a preprint server and are currently being peer reviewed.
The study findings underscore profound multi-cellular dysregulation in the brain caused by even mild respiratory SARS-CoV-2 infection. The white matter-selective microglial reactivity found in both mice and humans following SARS-CoV-2 infection have been shown to inhibit hippocampal neurogenesis, dysregulation of the oligodendroglial lineage and myelin loss in other disease contexts.
Myelin modulates the speed of neural impulse conduction and provides metabolic support to axons; even small changes in myelination can exert profound effects on neural circuit dynamics and consequently on cognitive function.
Considering these pathophysiological changes resulting from even relatively mild SARS-CoV-2 infection together with the additional neuropathological consequences that can occur in more severe systemic SARS-CoV-2 infection including microvascular thrombi, neuron loss, cortical inflammation, marked and persistent CSF cytokine elevation and even direct brain infection in some cases, it is not surprising that the neurological sequalae of COVID-19 infection are proving to be both common and debilitating.
SARS-CoV-2 infection results in a startling rate of persistent symptoms.
Long COVID or PASC (Post-Acute Sequelae of SARS CoV-2 infection) is thought to affect a high fraction of people who have recovered from SARS-CoV-2 infection. A meta-analysis of 45 studies involving nearly 10,000 subjects found that more than 70% of people experience at least one symptom lasting more than 2 months after infection, with cognitive dysfunction affecting 25% of people, even those who had mild SARS-COV-2 infection.
Alarmingly, in a study of patients in Italy with COVID-19 pneumonia requiring hospitalization in the spring of 2020, neuropsychometric testing revealed impairment in at least one cognitive domain in 78% of patients at 3-months post-infection, with frequent cognitive impairments affecting psychomotor coordination (57%), executive function (50%), attention and information processing speed (33%), working memory (24%) and verbal memory (10%).
Yet another neuropsychometric study examining all patients with mild, moderate or severe COVID-19 in a New York City hospital system, followed from spring of 2020 through spring of 2021, found impairment in attention (10%), processing speed (18%), memory encoding (24%) and executive function (16%) evident at 7 months after infection.
The incidence and severity of cognitive impairment following COVID-19 caused by newer SARS-CoV-2 variants such as the Omicron variant, or as a result of breakthrough infection in vaccinated individuals, remains to be determined but it is assumed to be the same if not worse.
Clinical similarities in the “COVID-fog” and “chemo-fog” syndromes of cognitive impairment, the findings here illustrate numerous pathophysiological similarities in the multi-cellular dysregulation evident following cancer therapies and following SARS-CoV-2 infection, including white matter microglial reactivity, dysregulation of neural precursor cell populations, reduction in hippocampal neurogenesis, depletion of myelinating oligodendrocytes and myelin loss.
Similar to after cancer therapies and in other disease states, the microglial reactivity present after mild respiratory SARS-CoV-2 infection could also induce neurotoxic astrocyte reactivity, as well as aberrant microglial pruning of synapses.
In the context of severe COVID, microglia in the human cerebral cortex exhibit a transcriptional phenotype that partially overlaps with the neurodegenerative disease-associated microglial phenotype, and cortical astrocytes exhibit a transcriptional program consistent with neurotoxic reactivity
Whether neurotoxic astrocyte reactivity, induced by the reactive microglia described above, occurs after mild respiratory COVID remains to be determined.
However, the oligodendrocyte loss observed here could be caused by such neurotoxic astrocyte reactivity, which is known to cause oligodendrocyte cell death. Microglial depletion strategies can restore similar multi-cellular deficits and rescue impaired cognitive performance in mouse models of cancer therapy-related cognitive impairment, it remains to be determined if similar therapeutic interventions will prove beneficial for cognitive impairment associated with COVID-19.
SARS-CoV-2 infection induces a broad inflammatory response, well beyond the typical type 1 immune response seen with other respiratory viral infections (Lucas et al., 2020).
The study team found that even mild SARS-Cov-2 infection can induce prominent elevations in CCL11, a chemokine known to impair mechanisms of neural plasticity and cognitive function, together with white matter-selective microglial reactivity in both mice and humans.
In long-COVID patients, most of whom experienced a relatively mild course with their initial SARS-CoV-2 infection, CCL11 was significantly elevated in those with “brain fog” symptoms. In mice, this persistent neuroinflammatory response is associated with impaired hippocampal neurogenesis and loss of both oligodendrocyte precursor cells and mature oligodendrocytes, neuropathological changes predicted by a wealth of previous preclinical work.
The effects of systemic inflammation on microglial reactivity and associated dysregulation of neural cells are not specific to COVID-19. Systemic exposure of rats to low levels of bacterial liposaccharide (LPS) – sufficient to cause mild-moderate sickness behavior but not sepsis, similarly causes microglial reactivity and impairment in hippocampal neurogenesis. People recovering from critical illness in general experience high rates of long-term cognitive impairment, and persistent cognitive impairment is an important component of postintensive care syndrome (PICS). Other viral syndromes such as influenza cause microglial reactivity and can impair cognitive function, even in the absence of neuroinvasion.
However, the particularly immunogenic nature of SARSCoV-2, together with the magnitude of people infected during this pandemic, contribute to the emerging crisis of persistent cognitive impairment associated with COVID-19 infection.
Neurological Long COVID issues is going to be a very common occurrence in vast amount of the populations and we can expect to see also more neuropsychiatric issues and also neurodegenerative issues fast becoming more predominant coupled with more excess deaths due to neurological issues such as strokes and cerebral venous sinus thrombosis (CVST).,-correlation-or-causal
Its definitely going to be fun days ahead.
Thailand Medical News is initiating our own studies in collaboration with other research institutions using herbs and phytochemicals to suppress neuroinflammation, assist with protecting the microgial and also help with regeneration of neurons and myelin with context of SARS-CoV-2 infections, those willing to support our initiatives can make a direct donation to us and you will be kept abreast of our findings and also a set of the end products we are developing. However, we have no intentions of making any of these publicly known or published as we only want to protect and support a small community of like-minded people who truly believe in what we are doing and are non-judgemental. Minimum donations accepted for this programme is set at US$300 and we only accept donors from America, Canada, Europe, Singapore, Australia and Japan.
For the latest on Long COVID or NEUROCOVID, keep on logging to Thailand Medical News.


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