COVID-19 Long-Term Brain Health Impact

COVID-19 could trigger a brain health time-bomb in the future. If so, what can we do now?
Amprion Blog - Covid Brain Fog - 1200 x 600
Amprion Blog - Covid Brain Fog - 1200 x 600
COVID-19 could trigger a brain health time-bomb in the future. If so, what can we do now?
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Once COVID-19 has passed with effective vaccines, could there be the aftermath of brain health-related issues triggered by the coronavirus, years or even decades after the initial infection? This is the root of our concern post the COVID-19 pandemic: The rise of neurodegenerative disease cases. The most common of these disorders are Alzheimer’s and Parkinson’s.

According to Nature and other creditable reports, we discover that hospitalized COVID-19 patients have significant neurological damage described clinically as confusion, cognitive decline, and “brain fog” for extended periods after the virus has disappeared. This article will discuss how the coronavirus damages the brain, historical data linked to the previous virus and bacterial infections, how big this post-COVID problem is, and what to do about it. Let’s dive in.

How does COVID-19 damage the brain?

There is some disagreement over whether the Covid-19 coronavirus can infect brain cells directly. However, there seems to be general agreement that Covid-19 infection causes widespread damage to blood vessels, including those in the brain, and disruption of the blood-brain barrier that normally protects the brain from neurotoxins and inflammatory agents circulating in the blood. One possible consequence is the triggering of long-term neurodegeneration leading to Alzheimer’s and Parkinson’s Disease.

The progression of Alzheimer’s and Parkinson’s to show clinical symptoms may take 20-30 years or more. Will we see an explosion of these cases in people exposed to Covid-19 twenty to thirty years from now?

Neurodegenerative disorders linked to previous virus infections

Alzheimer’s and Parkinson’s patients show increased association with the presence of certain viruses and bacteria.

  • Alzheimer’s patients have shown more cases of previous herpesvirus infection compared with other age-matched individuals. This evidence suggests that certain herpesviruses may trigger or accelerate a cascade of events that culminate decades later as Alzheimer’s.[A]
  • Similarly, there are claims that patients with Alzheimer’s show more significant evidence of the previous infection in the brain with cyanobacteria than typical peers.  [B]
  • There is also increasing evidence for both Alzheimer’s and Parkinson’s related to certain bacteria colonizing the gut, including cyanobacteria. [C and D]
  • Finally, several novel drugs in current pharma pipelines attempt to correct or slow these diseases by adjusting the intestines’ bacterial microbiome.[E]

How big is this problem potentially?

Up to 2 billion people worldwide could be infected with COVID-19 before a vaccine can reduce new infections. If only a small fraction of these patients develop Alzheimer’s or Parkinson’s, we could be looking at millions of COVID-linked cases by 2040 or 2050.

According to Nature, half of the hospitalized Covid-19 patients show neurological involvement. This development could conceivably add millions of people to the already increasing burden of neurodegenerative diseases.

Based on the estimated care cost per neurodegenerative disease patient at $250,000 annually in the US and Europe, we project the added economic burden could skyrocket to as high as $1 trillion or more annually.

Since the peak of infections now occurs in younger patients age 18-45, this is the population most at risk.

What can we do now? 

The COVID pandemic presents a unique opportunity to study the long-term effects of a systemic viral disease that appears to affect almost every organ and system in symptomatic individuals. There is much to be learned from long-term research on this population, especially those sick enough to be hospitalized.

Establish a COVID-19 global database and biorepository 

One highly effective way to learn from this pandemic and be more prepared for the next would be to set up a comprehensive global program to follow-up hospitalized and asymptomatic patients over 10-30 years. Here is a quick look at the who, why, what, when, and how:

Who?

Collect confidential clinical and demographic information from a cohort of between 10,000 and 100,000 hospitalized COVID-19 patients. This effort could be funded by a consortium of governments or by a private/public consortium.

Why?

We can uncover many essential links and correlations in the future through large datasets and machine learning algorithms.

What?

Collect, store, and track baseline samples from these patients and build a global biorepository. Samples collected should include blood whenever possible, plus spinal fluid if clinically indicated for hospitalized patients with neurological symptoms. We would use the biorepository for research purposes, following ethical and regulatory guidelines to address privacy concerns.

How?

We would store all test results from biorepository samples anonymously and in secured, publicly accessible databases. All of the repository analyses should be published, stored, and accessible online through a secured system.

When?

Enroll as many patients as possible in a voluntary monitoring program. Patients would include annual or biannual follow-up surveys and additional samples for the repository at 5 to 10-year intervals.

Potential benefits

The potential benefits are enormous, and the costs relatively low. If we detect no increase in neurodegenerative disease after 20-30 years, we can still track other chronic diseases, including cardiovascular, pulmonary, renal, autoimmune, and metabolic.

The potential impact on multiple chronic diseases

Suppose we observe a delayed increase in neurodegenerative disease or other chronic diseases in this cohort. In that case, we should use the biorepository to identify the earliest biomarkers of illness beginning at the time of infection and gain otherwise inaccessible information about these diseases’ initiation and progression. It is hard to imagine that this information would not identify novel targets for diagnosis and treatment.

Potential impact for future pandemics

The net benefit would be the global availability of a database and repository of highly diverse (concerning age, gender, nationality, genetics) patients, all indexed to a particular starting point in time and all exposed to a highly pervasive and infectious virus. In a manner analogous to a global-pandemic Framingham study, this cohort is likely to inform our knowledge of chronic diseases and pandemic consequences for much of the 21st century.

The risks of doing nothing

The main cost of doing nothing is a missed opportunity to build a synchronized cohort of patients likely to show an increased likelihood for a wide array of chronic diseases.

This cohort may help identify the earliest stages of the disease and various progression paths for neurodegenerative diseases.  Studying this cohort is also likely to shed new light on the effects of different genetic backgrounds on both the probability of developing disease after virus infection and the timing of chronic illnesses.

Since these are critically important questions, the downside is relatively low. However, the window of opportunity is closing due to the booming manufacturing and distribution of vaccines. We need leadership in the global biomedical community to step forward now. There is no time to waste.

Sources:

A.  Can Herpesvirus Increase Your Risk for Alzheimer’s Disease? Nick Meehan, August 26, 2019, https://www.alzdiscovery.org/cognitive-vitality/blog/can-herpesvirus-increase-your-risk-for-alzheimers-disease

B. (Algae Bloom Toxin Linked to Alzheimer’s, other Diseases, Amy Kraft, CBSNews, January 21, 2016, https://www.cbsnews.com/news/algae-bloom-toxin-linked-to-alzheimers-and-other-neurodegenerative-diseases/

C. The Relationship Between Parkinson’s Disease and the Microbiome, Practical Gastro, S. Steinberg, S. Hazan, J. Daniels, February 2020, https://practicalgastro.com/2020/03/13/the-relationship-between-parkinsons-disease-and-the-microbiome/

D. Med Hypotheses, 2013 Jan;80(1):103. Blue-green algae or cyanobacteria in the intestinal micro-flora may produce neurotoxins such as Beta-N-Methylamino-L-Alanine (BMAA), which may be related to the development of amyotrophic lateral sclerosis, Alzheimer’s disease, and Parkinson-Dementia-Complex in humans and Equine Motor Neuron Disease in horses

E. China Alzheimer Drug Seeks Global Legitimacy With U.S. Trial, Bloomberg News, November 4, 2020

 

 

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