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[COVID-19 Virus] The Sinkies are fucked Thread.
- Thread starter zhihau
- Start date
Genetic link between COVID-19 and Alzheimer’s identified
www.medicalnewstoday.com
Share on PinterestA new study finds a genetic bridge between Alzheimer’s and COVID-19. Nor Hasen/EyeEm/Getty Images
According to the World Health Organization (WHO)Trusted Source, over 55 million people live with dementia worldwide, and doctors diagnose 10 million new cases each year. Around 60–70% of these are Alzheimer’s cases.
Dr. Salih is a senior research associate in neurodegenerative disease at University College London (UCL).
In previous work by UCL, genetic studies revealed that different genes can alter the risk of developing Alzheimer’s disease. These “risk genes” change how microglia, or immune cells of the brain, respond to amyloid protein and tangles.
Scientists have focused on a subpopulation of microglia cells known as interferon response microglia (IRM)Trusted Source, which increase with age and in response to amyloid proteins.
IRM cells respond to interferon proteins that the body releases to fight viral infections, such as SARS-CoV-2.
According to Dr. Rosa Sancho, head of research at Alzheimer’s Research UK, “Fairy early in the pandemic, people with dementia emerged as a group at particular risk of severe COVID-19.”
The new study, led by Naciye Magusali, a doctoral candidate at UCL, focused on the genotyping of 2,547 human DNA samples. Of these, 1,313 were from people with a diagnosis of Alzheimer’s disease, and 1,234 were from controls without Alzheimer’s.
The authors identified a variant of the interferon-stimulated gene oligoadenylate synthetase 1 (OAS1) that can increase the risk of developing Alzheimer’s disease by an estimated 11–22%.
Scientists have also shown that OAS1, which regulates inflammatory proteins, contributes to the genetic riskTrusted Source associated with severe COVID-19 outcomes.
According to the current study, cells treated to mimic the effects of COVID-19 showed a lower expression of OAS1.
Dr. Salih explains: “The variant in OAS1 associated with disease is lowering OAS1 expression. This supports the idea that people with lower levels of OAS1 are more likely to show a chronic cytokine response or ‘cytokine storm.'”
The work shows that the body needs OAS1 to reduce the amount of inflammation-causing proteins. According to Dr. Salih:
“We see in […] microglial cells that OAS1 is suppressing pro-inflammatory function of cells in response to elevated levels of interferon.”
These findings show the importance of inflammation in both the progression of Alzheimer’s disease and the severity of COVID-19.
Speaking about the new research, Dr. Sancho points out that “[w]e don’t know whether the effects of this risk gene could influence long-term neurological consequences of COVID-19 or whether COVID-19 […] increases the risk of dementia later in life.”
Dr. David Strain, a senior clinical lecturer at the University of Exeter in the United Kingdom, comments: “It does add important information as to the pathogenesis of the more severe presentations of COVID-19 and will hopefully be able to shed further light on potential treatment options or even personalized preventive medicine.”
www.medicalnewstoday.com
- Scientists have identified a genetic link between the development of Alzheimer’s and severe COVID-19 outcomes.
- A new study identifies the same immune system changes in both diseases.
- Targeting specific “risk” genes could lead to future treatments for Alzheimer’s disease and COVID-19.
According to the World Health Organization (WHO)Trusted Source, over 55 million people live with dementia worldwide, and doctors diagnose 10 million new cases each year. Around 60–70% of these are Alzheimer’s cases.
Alzheimer’s disease and inflammation
“While Alzheimer’s is primarily characterized by a harmful buildup of amyloid protein and tangles in the brain, there is also extensive inflammation in the brain that highlights the importance of the immune system in Alzheimer’s,” explains Dr. Dervis Salih.Dr. Salih is a senior research associate in neurodegenerative disease at University College London (UCL).
In previous work by UCL, genetic studies revealed that different genes can alter the risk of developing Alzheimer’s disease. These “risk genes” change how microglia, or immune cells of the brain, respond to amyloid protein and tangles.
Scientists have focused on a subpopulation of microglia cells known as interferon response microglia (IRM)Trusted Source, which increase with age and in response to amyloid proteins.
IRM cells respond to interferon proteins that the body releases to fight viral infections, such as SARS-CoV-2.
According to Dr. Rosa Sancho, head of research at Alzheimer’s Research UK, “Fairy early in the pandemic, people with dementia emerged as a group at particular risk of severe COVID-19.”
OAS1 gene and inflammation
The current findings, published in the journal Brain, build on previous work by Dr. Salih.The new study, led by Naciye Magusali, a doctoral candidate at UCL, focused on the genotyping of 2,547 human DNA samples. Of these, 1,313 were from people with a diagnosis of Alzheimer’s disease, and 1,234 were from controls without Alzheimer’s.
The authors identified a variant of the interferon-stimulated gene oligoadenylate synthetase 1 (OAS1) that can increase the risk of developing Alzheimer’s disease by an estimated 11–22%.
Scientists have also shown that OAS1, which regulates inflammatory proteins, contributes to the genetic riskTrusted Source associated with severe COVID-19 outcomes.
According to the current study, cells treated to mimic the effects of COVID-19 showed a lower expression of OAS1.
Dr. Salih explains: “The variant in OAS1 associated with disease is lowering OAS1 expression. This supports the idea that people with lower levels of OAS1 are more likely to show a chronic cytokine response or ‘cytokine storm.'”
The work shows that the body needs OAS1 to reduce the amount of inflammation-causing proteins. According to Dr. Salih:
“We see in […] microglial cells that OAS1 is suppressing pro-inflammatory function of cells in response to elevated levels of interferon.”
These findings show the importance of inflammation in both the progression of Alzheimer’s disease and the severity of COVID-19.
Speaking about the new research, Dr. Sancho points out that “[w]e don’t know whether the effects of this risk gene could influence long-term neurological consequences of COVID-19 or whether COVID-19 […] increases the risk of dementia later in life.”
Dr. David Strain, a senior clinical lecturer at the University of Exeter in the United Kingdom, comments: “It does add important information as to the pathogenesis of the more severe presentations of COVID-19 and will hopefully be able to shed further light on potential treatment options or even personalized preventive medicine.”
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already used engine brake, foot brake and hand brake liao... how?
Leeleease all brakes step accelerator and crash onto Rochalie drive in the middle of the night.
aka emergency brake.
one of my kaki’s close friend was part of the statistic, just heard the news tonightanother 10 deaths added to the score... death toll at 172 now...
11 deaths recorded today, death toll at 183
wow....11 deaths.....and out of them 8 have had some sort of vaccination (part or full).
But Mrs Leetard said it's the pandemic of the unvaxxed....
Wow the Singapore numbers are quite different from the numbers here in Alberta.
Maybe the crowded city just means the virus spreads around a lot more.....
Which brings to......
You could be right that this might be an option down the road if the ICU gets overwhelmed. Won't say it is not a possibility in SG.
Ok i MAY BE WRONG here, it's just a hunch. Clarification, I am not antivax, I am just anti biased vax that's all. Regarding reports of the P vax efficacy waning after about 6mths, if I use the hypothesis of those who were the first fatalities in majority, were they not the seniors? Why I suggest that. Cause they were the 1st to get 1 or both doses.
Now, if we follow the trend, hasn't it been fatalities that are getting younger & younger in terms or age group from the seniors coming downwards, thus they are now suggesting even age 50+ get a 3rd shot?
Make sense?
Now, if we follow the trend, hasn't it been fatalities that are getting younger & younger in terms or age group from the seniors coming downwards, thus they are now suggesting even age 50+ get a 3rd shot?
Make sense?
If I recalled correctly, healthcare workers and front-line staff got their shots in Jan/Feb period, followed by the elderly as well as those folks who are immunocompromised in March.
No words are necessary.
The one on right in that interview said that we closed our borders last year because cases overseas were high.
Now cases overseas have stablized, and our cases are high, so we can open our borders.
The logic is weird.
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Canada published this information a few days ago.
Protection is very high if both doses are spaced 8-16 weeks apart.
Even with single dose, protection is very high.
It is bewildering that our local partially-vaccinated account for a high % in the daily death counts.
It is bewildering that our local partially-vaccinated account for a high % in the daily death counts.
First group was mandatory, old farts were 'invited' with personal letters. Immunocompromised, children and preggies etc were all told to stay away in their vaccination propaganda. That all changed later.
How quickly Sinkies forget.
See the transition:
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