COVID-19 Linked to Increased Dementia Risk: Fulfills Bradford Hill Criteria for Neuronal Damage

According to a new study, getting infected with COVID-19 may significantly increase the chance of getting dementia. This meets the Bradford Hill criteria for proving causation. This new information shows how SARS-CoV-2 affects brain health in the long run.

Damage to nerve cells and Covid-19

The point-of-view piece in The Lancet Neurology by Bonherry et al. from Europe and Australia clearly shows that COVID-19 is linked to neurodegenerative illnesses. It's important to note that infectious diseases like COVID-19 increase the number of infections, which is known to make illnesses like dementia more likely. A study found that the chance of getting dementia goes from 1% to 1.5% after getting SARS-CoV-2.

Alzheimer's and other neurodegenerative diseases may be more likely to happen if you live in certain places or have specific genes. The Lancet Commission on Dementia has already found 12 things that put people at risk for dementia and can be changed.

One of these is how memory and confusion can make each other worse. However, the new study directly examines the risk of dementia after COVID-19 infection, an important area that hadn't been studied before.

Proof of Damage to Neurons

People who have Covid-19 often get brain problems like stroke, headaches, anosmia, dysgeusia, seizures, and Guillain-Barre syndrome. Also, these people are more likely to have psychiatric problems.

Scientists have made organoids from human pluripotent stem cells (hPSCs) that show SARS-CoV-2 can quickly attack brain and spinal cord cells. Even with these findings, the virus doesn't have the same effect on all neurons.

In a similar study, models made from hPSCs were used to look into how dopamine (DA) neurons react to SARS-CoV-2. They found that the virus can infect DA neurons, especially those with the A9-like subtype that is found in the substantia nigra (a part of the brain that is badly affected in Parkinson's disease). This finding is important because it connects COVID-19 to a possible cause of Parkinson's disease (PD) by making DA neurons age faster.

The study also found that molecules change when DA neurons are infected with SARS-CoV-2. For example, proteins like LMO3 are expressed more, and CALB1 is expressed less. This illness can cause neuronal senescence, which worsens neurodegenerative processes.

What It Means and Future Research

These results are significant because they show that COVID-19 may have neurological effects that last longer than the short-term symptoms. It is essential to monitor COVID-19 people for signs of neurodegenerative diseases like Parkinson's disease and dementia. The study's findings show that the virus can raise amounts of α-Syn, a protein linked to Parkinson's disease, which speeds up the breakdown of neurons.

Researchers found that drugs like riluzole, imatinib, and metformin could stop the aging of DA neurons caused by SARS-CoV-2. We can find new ways to treat the fever. These medicines prevent the virus from getting in and start signaling pathways that guard. However, they must be studied more to see how well they stop neurological effects after a COVID-19 infection.

As shown by Bonherry et al. and other studies, there is a clear link between COVID-19 and a higher chance of getting dementia. The long-term effects of COVID-19 on the nervous system need to be closely watched and thoroughly studied right away because these results meet the Bradford Hill criteria for cause. Awareness of and lowering these risks will become more critical as the pandemic continues. This is to protect brain health and deal with the more significant effects of SARS-CoV-2.