RE: Long Covid - 14

Viruspersistenz im Knochenmark wird hier als Auslöser spekuliert. Jemand Ideen wie dies eventuell anzugehen wäre im Knochenmark?

Altered mitochondrial respiration in peripheral blood mononuclear cells of post-acute sequelae of SARS-CoV-2 infection
https://www.sciencedirect.com/science/ar...567724924000072


Im Grunde würde dieses Paper auch in das Thema Junges Blut passen.

Dysregulated platelet function in patients with postacute sequelae of COVID-19
https://journals.sagepub.com/doi/10.1177/1358863X231224383

#326 Ich würde bei Long Covid generell versuchen über das Immunsystem und antivirale Mittel zu gehen.

Ursache von Long Covid: Virusschrott von Sars-CoV-2 kann anhaltende Entzündungen auslösen
https://web.de/magazine/wissen/wissensch...loesen-39316850

P2X3 Antagonisten werden hier als mögliche Optionen genannt. Das ist übrigens auch mit einigen natürlichen Substanzen möglich und nicht nur mit dem im Paper erwähnten Gefapixant.

Carotid body dysregulation contributes to Long COVID symptoms
https://www.nature.com/articles/s43856-024-00447-5

Wäre eventuell eine Möglichkeit bzgl. des Problems mit der Blut-Hirn-Schranke.

Beta-caryophyllene inhibits the permeability of the blood–brain barrier in MPTP-induced parkinsonism
https://www.sciencedirect.com/science/ar...213485323000324

Blood–brain barrier disruption and sustained systemic inflammation in individuals with long COVID-associated cognitive impairment

Zitat

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Vascular disruption has been implicated in coronavirus disease 2019 (COVID-19) pathogenesis and may predispose to the neurological sequelae associated with long COVID, yet it is unclear how blood–brain barrier (BBB) function is affected in these conditions. Here we show that BBB disruption is evident during acute infection and in patients with long COVID with cognitive impairment, commonly referred to as brain fog. Using dynamic contrast-enhanced magnetic resonance imaging, we show BBB disruption in patients with long COVID-associated brain fog. Transcriptomic analysis of peripheral blood mononuclear cells revealed dysregulation of the coagulation system and a dampened adaptive immune response in individuals with brain fog. Accordingly, peripheral blood mononuclear cells showed increased adhesion to human brain endothelial cells in vitro, while exposure of brain endothelial cells to serum from patients with long COVID induced expression of inflammatory markers. Together, our data suggest that sustained systemic inflammation and persistent localized BBB dysfunction is a key feature of long COVID-associated brain fog.

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https://www.nature.com/articles/s41593-024-01576-9

#331
Daher auch bewusst das Paper erwähnt in #330. Das Problem mit der Blut-Hirn-Schranke muss ja auch gefixt werden damit nicht noch mehr Schaden entsteht.

Zitat von Speedy im Beitrag #332

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#331
Daher auch bewusst das Paper erwähnt in #330. Das Problem mit der Blut-Hirn-Schranke muss ja auch gefixt werden damit nicht noch mehr Schaden entsteht.

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Sex differences in symptomatology and immune profiles of Long COVID
https://www.medrxiv.org/content/10.1101/...2.29.24303568v1

Iron dysregulation and inflammatory stress erythropoiesis associates with long-term outcome of COVID-19
https://www.nature.com/articles/s41590-024-01754-8

Role of the complement system in Long COVID
https://www.medrxiv.org/content/10.1101/...3.14.24304224v1

COVID’s toll on the brain: new clues emerge
A leaky blood–brain barrier and inflammation might account for some of the cognitive symptoms of COVID-19.
https://www.nature.com/articles/d41586-0...obox=1710951189

Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID
https://www.nature.com/articles/s41538-024-00261-2

Brain exposure to SARS-CoV-2 virions perturbs synaptic homeostasis
https://www.nature.com/articles/s41564-024-01657-2

Der reversible Kaliumkanal Blocker Amifampridin soll laut ersten Erfahrungsberichten (Off-Label Einsatz) recht deutliche Erfolge vor allem hinsichtlich Fatigue zeigen.

Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches
https://link.springer.com/article/10.1007/s11357-024-01165-5

The tryptophan catabolite or kynurenine pathway in Long COVID disease: A systematic review and meta-analysis
https://www.medrxiv.org/content/10.1101/...4.30.24306635v1

Aktueller Tweet von Carmen Scheibenbogen:

"Antikörper verursachen Long COVID Symptome! @PutrinoLab zeigte in seinem Vortrag, dass Antikörper von LC Patienten, die Mäusen gespritzt werden, Muskelschwäche und Schmerzempfindlichkeit übertragen".

Persistent Activation of Chronic Inflammatory Pathways in Long Covid
https://www.biorxiv.org/content/10.1101/2024.05.11.593709v1

Diese Pathways müsste man dann gezielt angehen. Allerdings parallel auch die Viruspersistenz natürlich denn ansonsten bewegt man sich ja im Kreis.

Investigation into the restoration of TRPM3 ion channel activity in post-COVID-19 condition: a potential pharmacotherapeutic target
https://www.frontiersin.org/journals/imm...24.1264702/full

Diverse immunological dysregulation, chronic inflammation, and impaired erythropoiesis in long COVID patients with chronic fatigue syndrome
https://www.sciencedirect.com/science/ar...89684112400101X

HISTOLOGICAL AND ULTRASTRUCTURAL CHANGES IN LUNGS ONE YEAR POST ASYMPTOMATIC OR MILD SARS-COV-2 INFECTION: EVALUATING THE POTENTIAL FOR ACTIVE VIRUS PRESENCE
http://www.intjmorphol.com/abstract/?art_id=10675

Substance P – a regulatory peptide with defense and repair functions. Results and perspectives for the fight against COVID-19
https://www.frontiersin.org/journals/neu...24.1370454/full

Altered brain perfusion and oxygen levels relate to sleepiness and attention in post-COVID syndrome
https://onlinelibrary.wiley.com/doi/10.1002/acn3.52121

A causal link between autoantibodies and neurological symptoms in long COVID
https://www.medrxiv.org/content/10.1101/...6.18.24309100v1