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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WHY INFECTIONS by BACTERIA, VIRUSES and FUNGI will INCREASE in the FUTURE ? π§΅
2 recent studies highlights important concerns about the rise of infections caused by bacteria, viruses, fungi and the role of COVID-19
2) One study focuses on antibiotic resistance, where bacteria become resistant to medicines meant to kill them. This often happens due to the overuse of antibiotics in healthcare and agriculture, along with a lack of new antibiotics being developed.
3) As these bacteria evolve and become harder to treat, even common infections could lead to severe health problems.
The second study discusses how climate change and urban growth are contributing to the increase in viral and fungal infections.
2) Astrocytes are the brain cells that can be infected and support the growth of the SARS-CoV-2 virus. This likely contributes to the neurological symptoms of COVID-19.
3) Experiments show ketamine, an anesthetic, can reduce astrocyte infection by earlier SARS-CoV-2 variants, but not newer variants. Ketamine does this by decreasing the virus's entry receptor and replication in astrocytes.
2) This first figure helps explain the first key mechanisms contributing to cognitive impairment in COVID-19 patients:
βΆοΈ Direct viral entry and brain injury is shown in the first panel.
βΆοΈ The role of hypoxia (lack of oxygen) in cognitive decline is depicted in the second panel
3) βΆοΈ The widespread systemic inflammation caused by COVID-19 is illustrated in the third panel.
For CHILDREN, the risk of LONG COVID after a SECOND INFECTION is 2.08 TIMES GREATER compared to the FIRST INFECTION. medrxiv.org/content/10.110β¦
2) Let's summarize first this study :
The researchers used medical records from 40 children's hospitals in the US between January 2022 and October 2023. They compared the risk of long-term issues in those with a second COVID-19 infection versus their first infection.
3) Results showed that children with a 2nd infection had a significantly higher risk of various long-term problems, including:
- Heart issues like inflammation and abnormal heart rhythms
- Changes in taste and smell
- Blood clots
- Kidney problems
- Fatigue and muscle/joint pain
What a "CLEVER" SARS-COV-2 virus !
... which induced a P812S mutation in a chronically ill individual, that is somewhat less pathogenic but enables the virus to infect a larger population. biorxiv.org/content/10.110β¦
2) This study looks at how a single mutation, called P812S, in the SARS-CoV-2 virus can have different effects. The P812S mutation was found in a person with a long-term COVID-19 infection.
3) The study found that the P812S mutation:
- Reduced the ability of the virus to enter cells and cause them to fuse together (form syncytia). This is linked to less severe COVID-19 disease.
- Helped the virus evade antibodies that target the fusion peptide region of the spike.