2) COVID-19 and Parkinson's disease (PD) may be linked through shared mechanisms like neuroinflammation, oxidative stress, autophagy dysregulation, and ACE2 downregulation. SARS-CoV-2 infection could trigger pathways involved in PD development.
3) Analysis of gene expression data identified differentially expressed genes (DEGs) between PD/COVID-19 and controls. Pathway analysis showed genes were involved in processes like inflammation and immune response.
4) Ibuprofen may help alleviate PD and COVID-19 by inhibiting the NF-ΞΊB signaling pathway through DEGs like RELA. This pathway is activated in both diseases and involved in inflammation.
5) ACE2 plays a role in PD pathology based on a mouse model with ACE2 knockout. These mice showed worse PD symptoms, more neuronal loss, and increased inflammation markers. ACE2 is expressed in brain areas implicated in PD.
6) SARS-CoV-2 entry involves binding to ACE2 receptor. Downregulating ACE2 during COVID-19 could impact pathways involved in both diseases and exacerbate symptoms
7) Inflammation, oxidative stress, autophagy and mitochondrial dysfunction are shared mechanisms that may amplify adverse effects when PD and COVID-19 interact. Further research is needed to validate models of this interaction.
8) In summary, the paper investigates potential links between COVID-19 infection and increased PD risk or severity based on overlapping molecular pathways, and identifies ACE2 and NF-ΞΊB inhibition as potential targets for further study.
Thanks for reading π
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NIPAH VIRUS
Jumping to conclusions during outbreaks only fuels panic and misunderstanding; NOT EVERY VIRUS OUTBREAK is a PANDEMIC.
We raised the alarm about Nipah in 2023, but itβs essential not to confuse an epidemic related to this virus, ...
2) ...like the one in India, with a pandemic risk or a situation like COVID-19.
Nipah virus is transmitted primarily from animals, especially bats, to humans. It spreads through direct contact with infected animals, their secretions, or contaminated foods.
3) Human-to-human transmission occurs only through close contact, such as touching or caring for an infected person, as well as sharing fluids like saliva or blood.
We cannot equate a virus transmitted through fluids with a respiratory virus like SARS-CoV-2.
"70% to 90% of our CELLS are completely RENEWED in less than 5 YEARS!
So If weβre mostly "New", why are so many still struggling with SARS-CoV-2?
We will tackle this question, which is more complex than it seems, in several posts.
2) First, let's say a few words about cell renewal.
70% to 90% of our cells are renewed over time. This turnover occurs in various cell types, including skin, blood, and immune cells, allowing the body to replace damaged or aged cells. sciencefocus.com/the-human-bodyβ¦
3) For instance, red blood cells have a lifespan of about 120 days, while skin cells regenerate every few weeks.
Even with significant cell renewal, aging persists due to changes in our DNA. sciencefocus.com/the-human-bodyβ¦
2) Co-infection occurs when a person is infected by more than one virus at the same time. This can lead to interesting and sometimes complex interactions between the viruses
3) In one study about SARS-CoV-2, researchers found that when different versions of this virus infect the same person, they can mix their genetic material through a process called recombination. This means that the new version of the virus can have traits from both parent viruses
For more than three years, we have been emphasizing that the envelope protein is an essential component and that we cannot limit our focus to just the spike protein. We are now uncovering its role in long COVID.
3) The Envelope (E) protein of SARS-CoV-2 plays a crucial role for several reasons:
βΆοΈ Virus Assembly and Release: The E protein is essential for the virus's assembly and budding from infected cells, contributing to its stability and infectivity.
"N''oubliez jamais" (Never forget - Joe Cocker)π§΅
In 2022, COVID-19 was the second leading cause of death globally, with the repercussions of the virus far from over. The lasting impact of the pandemic continues to affect lives around the world.
Recent research may have identified a key factor contributing to long COVID: microscopic clots intertwined with immune system debris in the blood. These unusual structures were found to be nearly 20 times more prevalent ...
2) ...in long COVID patients compared to healthy individuals. The clots, associated with neutrophil extracellular traps (NETs), suggest a potential biological marker for persistent symptoms.
3) These microclots could impede blood flow in small vessels, leading to issues like brain fog, fatigue, and shortness of breath.