A genetic link between COVID-19 and Alzheimer’s identified

0


Share on Pinterest
New study finds genetic bridge between Alzheimer’s disease and COVID-19. Ni Hasen / EyeEm / Getty Images
  • Scientists have identified a genetic link between the development of Alzheimer’s disease and the severe consequences of COVID-19.
  • A new study identifies the same changes in the immune system in both diseases.
  • Targeting specific ‘at risk’ genes could lead to future treatments for Alzheimer’s disease and COVID-19.

Alzheimer’s disease is the most common form of dementia, a syndrome in which cognitive function gradually declines over time.

According to World Health Organization (WHO), more than 55 million people suffer from dementia worldwide, and doctors diagnose 10 million new cases each year. About 60 to 70% of them are cases of Alzheimer’s.

Stay informed with live updates on the current COVID-19 outbreak and visit our coronavirus hub for more advice on prevention and treatment.

“While Alzheimer’s disease is primarily characterized by a harmful build-up of amyloid proteins and tangles in the brain, there is also significant inflammation in the brain which highlights the importance of the immune system in Alzheimer’s disease. “, Explain Dr Dervis Salih.

Dr Salih is Senior Research Associate in Neurodegenerative Diseases at University College London (UCL).

In previous work by UCL, genetic studies found that different genes can alter the risk of developing Alzheimer’s disease. These “risk genes” change the way microglia, or immune cells in the brain, respond to amyloid protein and tangles.

Scientists focused on a subpopulation of microglial cells called response to interferon microglia (MRI), which increase with age and in response to amyloid proteins.

MRI 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 at the start of the pandemic, people with dementia emerged as a particular risk group for severe COVID-19. “

Current results, published in the journal Brain, build on previous work by Dr. Salih.

The new study, led by Naciye Magusali, a doctoral student at UCL, focused on the genotyping of 2,547 human DNA samples. Of these, 1313 were from people diagnosed with Alzheimer’s disease and 1234 were from controls without Alzheimer’s disease.

The authors identified a variant of the oligoadenylate synthetase 1 gene stimulated by interferon (OAS1) which may increase the risk of developing Alzheimer’s disease by approximately 11–22%.

Scientists have also shown that OAS1, which regulates inflammatory proteins, contributes to the genetic risk associated with serious consequences of COVID-19.

According to the present study, cells treated to mimic the effects of COVID-19 showed lower expression of OAS1.

Dr Salih Explain: “The variant in OAS1 associated with the disease decreases OAS1 expression. This supports the idea that people with high levels of OAS1 are more likely to have a chronic response to cytokines or ‘cytokine storm. ‘”

Work shows that the body needs OAS1 to reduce the amount of protein causing inflammation. According to Dr Salih:

“We see in […] microglial cells that OAS1 suppresses the pro-inflammatory function of cells in response to high levels of interferon.

These results show the importance of inflammation in both the progression of Alzheimer’s disease and the severity of COVID-19.

Speaking of the new research, Dr Sancho points out this “[w]We don’t know if the effects of this risk gene could influence the long-term neurological consequences of COVID-19 or if COVID-19 […] increases the risk of dementia later in life.

Dr David Strain, clinical lecturer at the University of Exeter in the United Kingdom, comments: “This adds important information as to the pathogenesis of the more severe presentations of COVID-19 and, hopefully, may shed light on potential treatment options or even personalized preventive medicine.”

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.



Leave A Reply

Your email address will not be published.