Covid-19 is a disease that affects multiple organs. Even after the causative virus is no longer detectable by diagnostic tests, up to a third of patients suffer symptoms, often collectively called long Covid. There are around 200 symptoms of long Covid, but little consensus on how to detect or treat it.
Symptoms associated with brain function that linger for months after Covid-19 include fatigue, headaches, cognitive issues such as “brain fog”, anxiety, trouble sleeping, and post-traumatic stress disorder. Loss of taste and smell and reduced vision have also been reported. Not only do those with moderate or severe Covid-19 risk suffering from long Covid, even those with asymptomatic infections can experience it.
Clinical signs include abnormal Magnetic Resonance Imaging scans, bleeding of small blood vessels in the brain, inflammation, tissue damage from low oxygen-levels, and blood clots. Changes to brain structures and disruptions to blood vessels have been found in postmortem brain tissues of those who died from Covid-19.
At the time of writing, there have been no reports of virus particles infecting brain tissues. But we do know that Sars-CoV-2 infects sensory nerve cells.
Right now, there are a half dozen or so credible theories as to how long Covid develops and persists. One of these theories is that virus persists in nerve cells at very low levels below detection. But we do not know how long damage to the brain lasts. Even fifteen months after the pandemic was declared, there is much to learn about Covid-19.
That said, Covid-19 isn’t the first infectious disease that causes harm to the brain. Ebola, Zika, SARS, and MERS have all been linked to post-infection brain disorders. Prolonged loss of smell and taste have been linked to problems with long-term brain function for many other infections too. What is different is the scale of infections this time. Hundreds of millions of people have suffered from Covid-19. Even if a fraction suffers from brain disorders, it is a cause for alarm.
The H1N1 influenza pandemic of 1918-1919 is also suspected of causing a spike in depression, psychotic illnesses, sleep disorders, and a form of encephalitis. Over a century later, a definitive mechanism for how many of these brain disorders occurred has not been established.
At the Alzheimer’s Association International Conference in Denver, United States, in July, researchers discussed new findings on Covid-19 and dementia. Some biomarkers of brain injury, dementia, and inflammation have been found in elderly patients with severe Covid-19. Because of the similarity to Alzheimer’s, some researchers have dubbed this long Covid condition in elderly patients as “Alzheimer’s-like syndrome”.
Alzheimer’s disease affects millions of people worldwide. It causes short-term memory loss, mental decline, problems with speech, and difficulty in performing routine activities. Most cases occur in people above the age of 60.
The current scientific consensus is that Alzheimer’s disease is caused by accumulation of tell-tale protein plaques and tangles inside the brain. Tangles are clumps of a protein called tau. Plaques form from deposits of amyloid peptide, which is a shortened version of a protein found in nerve cells. The disease causes irreversible and progressive brain damage and can be clinically identified. But despite decades of research, the causes of the build-up of plaques and tangles remain unknown. Alzheimer’s remains an enigmatic disease.
For many years, the idea that infections might play a part in the progression of Alzheimer’s disease was not widely accepted. However, there is now mounting evidence of the involvement of pathogens in at least some cases of Alzheimer’s disease. Some of these pathogens infiltrate the brain directly and can cause chronic infections that trigger plaque formation.
For example, Herpes simplex virus-1 is a virus that causes some cases of herpes. It can remain in a dormant state in parts of the nervous system. Infections are often asymptomatic, but the virus can be reactivated. Some patients with herpes show symptoms of Alzheimer’s disease.
Revealingly, herpes virus DNA has been found in plaques from postmortem brain tissue samples of some patients with Alzheimer’s. Last year, researchers generated a model of Alzheimer’s disease in tissues with herpes virus. Still, the debate continues; some scientists think the virus makes the disease develop more rapidly instead of causing it in the first place.
Does Covid-19 cause dementia? Researchers have been careful to state that it is too early to draw definitive conclusions on long-term consequences of Covid-19. The extent of brain damage after Covid-19 and how long it lasts is not known and may vary from person to person depending on health, severity, age, and other factors.
Studies are currently underway. Some people may need to be tracked for 10-15 years to see if they have a greater chance of developing Alzheimer’s and other neurodegenerative diseases. And even if these diseases occur at a higher frequency in those who suffered from Long Covid, it may be hard to conclude that Sars-CoV-2 was a causative agent instead of a mitigating factor that pushed the disease further along.
But for anyone still on the fence about get vaccinated because their risk of dying from Covid-19 is low, the emerging details of brain dysfunction in long Covid are roundly convincing.
Anirban Mahapatra, a microbiologist by training, is the author of COVID-19: Separating Fact From Fiction
The views expressed are personal
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