COVID-19 Could Increase Dementia, Other Brain Disorders for

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COVID-19 Could Increase Dementia, Other Brain Disorders for Decades to Come

This article was published in Newsweek online 2/10/21. It has an interesting discussion of how Covid attacks the brain. I think you will enjoy reading it. I'll post some excerpts and link below.

https://www.newsweek.com/2021/02/19/covid-19-...67649.html

Loss of smell, emotional detachment and other cognitive disorders among COVID-19 survivors has in recent weeks become an urgent medical issue. Some patients experience psychotic breaks. Others report strange neurological symptoms—tremors, extreme fatigue, phantom smells, dizziness and bouts of profound confusion, a condition known as "brain fog." In one early study of more than 200 patients in Wuhan, neurological complications were identified in 36 percent of all cases and in 45 percent of severe cases. Another study in France in the New England Journal of Medicine reported neurological symptoms in 67 percent of patients.

Although it's too early to tell what the long-term effects of COVID-19 will be on the cognitive health of survivors, scientists now fear the disease could feed a spike in dementia and other neurodegenerative diseases in the decades ahead. In addition, a growing number of COVID long-haulers already meet the clinical criteria for Chronic Fatigue Syndrome (CFS), a mysterious condition, also called myalgic encephalomyelitis, characterized by extreme fatigue, exercise intolerance and a whole host of other strange and debilitating neurological symptoms. Prior to COVID-19, CFS afflicted 2 million Americans.

Neuroscientists, meanwhile, are doing what they can and focusing their efforts on ways of intervening early in the onset of COVID-19 with treatments that minimize long-term damage to the brain. Once patients have lived for months or even years with the syndrome, treatment is more difficult. "That's what we'd like to avoid," says Dr. Walter Koroshetz, director of NINDS. "The sooner you can intervene, the greater effect your intervention is likely to have. People who are two and three years out and are still sick, it's a tougher road.

There are competing theories as to what might be causing the damage to the brain in COVID-19, but so far scientists are most concerned about two: viral infection and autoimmune reactions. The two are not mutually exclusive, and there could be other causes that vary from case to case.

The most ominous possibility is that SARS-CoV-2 takes up residence in brain cells, which appears to be the case in other viral diseases associated with chronic neurological problems. That would make it more likely that, over the long run, the COVID-19 virus might contribute to neurodegenerative conditions. Studies of large populations of people suggest a link between common viral infections, such as herpes simplex virus and the molecular level processes seen in Alzheimer's disease and dementia, says neuroscientist De Erausquin. Studies also show that some viruses burrow into the brain, lie dormant for a time and eventually reemerge.

Scientists have recently found another reason to fear the brain effects of COVID-19. Although it was originally thought to be primarily a respiratory disease, it's now known to share some similarities with cancer in that it has the ability to metastisize, says Dr. Carlos Cordon-Cardo, director of the department of pathology at Mount Sinai Health System in New York City. It uses its famous spike-like proteins like grappling hooks to glom onto ACE2 receptors that are present in many types of human cells.

"The virus, even though it enters through the nose, can reach the lungs, the kidney, the liver, and now the brain because it goes into the blood vessels, it circulates, it travels into these tunnels," says Cordon-Cardo. "And then it can meet in a specific site to produce an extent of organ damage."

Nath suspects some long-haul symptoms might be explained by a hypothesis he favors for the cause of Chronic Fatigue Syndrome: The infection has left its victims with a persistent activation of the immune system, which has pushed the body into a low-level state of war with itself. Indeed, the many ways acute COVID-19 manifests in patients can be explained by how each individual's immune system reacts to the disease. The same may well be true in those suffering from chronic symptoms.

These two hypotheses for long-haul COVID-19—autoimmunity and direct brain infection—are "not mutually exclusive," Yale's Iwasaki notes.

Destruction of the outer lining of tiny capillaries in the brain, which has been spotted in a number of autopsies, could break down the blood-brain barrier, cause leakage, lead to blood clots and cause the whole brain to swell up "almost like a sponge put in water."

"That in itself is a problem because that allows things that are not supposed to go into the brain and the blood to actually get in, and that can set up problems in terms of the function of the brain tissue," Koroshetz says. "It also brings in an inflammatory response to kind of sop up the injury or sop up the proteins that are getting in that shouldn't be there."

In addition to pathogens, this breakdown can allow the unchecked infiltration of white blood cells, which Koroshetz describes as the "tanks" of the immune system, because they attack infected areas with far more firepower and far less specificity than the COVID-specific antibodies, which are the "guided missiles" of the immune arsenal.

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