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Can Covid-19 trigger Alzheimer’s disease?

5.7 min readPublished On: 17. December 2021By Categories: Causes, Infections, Prävention, prevention

It is now known in Alzheimer’s research that infection by certain bacteria and viruses may be associated with the development of Alzheimer’s disease, and that these microorganisms may therefore be a risk factor.

But does the new SARS-CoV-2 coronavirus also impact the brain and impairs cognitive function?

The question seems justified, since people often lose their sense of taste and smell after infection with the coronavirus, which means that SARS-CoV-2 obviously invades structures of the nervous system.

In this context, researchers discovered that Corona virus enters the central nervous system via the olfactory bulb (1). The olfactory bulb is a neural structure of the forebrain involved in olfactory perception, i.e. the sense of smell. From there, olfactory information is transmitted to deeper brain regions for processing, via the orbitofrontal cortex to the amygdala and hippocampus. These brain areas play a crucial role in emotions, memory and learning. Corona virus could also reach these areas via the trans-synaptic pathway (i.e., via the connections between neurons) after it has infected the olfactory bulb. These are precisely the regions that are typically affected in Alzheimer’s disease.

In addition to the well-known smell and taste abnormalities, ‘brain fog’ is also a common symptom of Covid-19 infection. Other symptoms range from headaches, anxiety, depression, hallucinations and vivid dreams to strokes and seizures. One study found that neurological complications occurred in more than 80% percent of Covid-19 patients studied (2). Further, a University of Michigan study shows that of 150 hospitalized Covid-19 patients, more than 70% experienced delirium, an extreme state of mental confusion and agitation, despite heavy sedation (3).

Because this growing evidence of the central nervous system consequences of SARS-CoV-2 raises important questions about its impact on the risk of subsequent cognitive decline, Alzheimer’s disease, and other dementias, researchers are calling for a global study program aimed to better understand the long-term effects of Covid-19 on the central nervous system (4).

Do these symptoms make the brain more susceptible only to Alzheimer’s or other long-term cognitive problems?

Cleveland Clinic researchers have identified, in parallel to the inflammatory alterations, some physiologic changes in Covid19 patients that are also seen in Alzheimer’s disease and other types of dementia (5). The study showed that specific Alzheimer’s markers responsible for inflammation of the brain were significantly altered by the SARS-CoV-2 infection. Also, certain viral factors were greatly increased in the cells of the blood-brain barrier. These results suggest that the virus may influence several signaling pathways involved in neuronal inflammation (neuroinflammation) and damage to the small blood vessels in the brain, which would explain the Alzheimer’s-like cognitive impairments.

Furthermore, the researchers found in this study that people with the genetic variant ApoE, a genetic risk factor for Alzheimer’s disease, have less active antiviral resistance genes and they are therefore less protected against Covid-19.

How exactly does SARS-CoV-2 get into the nerve cells?

It has long been known that SARS-CoV-2 enters the cells of the lower respiratory tract through a molecular entry port called the angiotensin-converting enzyme-2 (ACE2) receptor. Nerve cells in the brain (neurons) and the astrocytes (cells in the brain and spinal cord that support and protect neurons) also have these ACE2 receptors and could be affected by the virus, as demonstrated by experiments in cell cultures. Back in 2020, a group of researchers suggested that a specific surface receptor called Neuropilin1 (NRP1), which occurs on nerve cells in the brain and olfactory tract, could also play an important role (6): The surface protein of SARS-CoV-2, also called Spike-protein, can be cleaved by an endogenous enzyme called Furin, which occurs in the respiratory tract. This creates a smaller protein that can bind to the NRP1 receptor and thus open a pathway for the virus into the cell. This could make it easier for SARS-CoV-2 to enter cells that have a receptor for NRP1 on their surface in addition to ACE2. NRP1 is produced in many human tissues including the respiratory tract, blood vessels and neurons. A particularly high concentration is found in the olfactory epithelium. Cell entry via NRP1 could be responsible, especially in the case of SARS-CoV-2, for why the broad range of neurological symptoms occurs during infection. But whether SARS-CoV-2 actually takes this route has not been definitively clarified.

But what is already known for sure about the connection with Covid-19 and Alzheimer’s disease?

SARS-CoV-2 infection can trigger a massive release of inflammatory messengers such as cytokines, chemokines and other inflammatory signals, which can lead to disruption of the blood-brain barrier, injury to astrocytes, activation of microglia (immune cells of the brain) and thus neuroinflammation and neuron death (7). Prolonged inflammation in the brain can lead to the formation of the plaques typical of Alzheimer’s disease due to the over-activation of microglia (immune cells in the brain). In this way, the immune response and excessive inflammation in Covid-19 may also accelerate the progression of inflammatory neurodegeneration of the brain; older people are more susceptible to severe dementia courses after SARS-CoV-2 infection.

All this shows us how important it is to protect oneself against infection with SARS-CoV-2, but also to strengthen the body at the same time through a healthy lifestyle and thus to well arm it against such a viral attack. After all, if the virus encounters an immune-healthy ‘host’, the chances of a milder course of the disease and also the possible effects on brain health are certainly more favorable!

Conclusion:

The results of current studies are far from definitive and there are still many unanswered questions about the role of Covid-19 in the development of Alzheimer’s disease. However, there is little doubt now that the virus gains access to the central nervous system via the olfactory epithelium and can trigger neuronal symptoms such as brain fog and other cognitive complications. Since carriers of the ApoE4 genetic variant may be less protected from Covid-19, those with a family history of Alzheimer’s disease should be especially protective against SARS-CoV-2 infection. But it would be wrong to panic at this point, as this in turn leads to the release of stress hormones, which in turn down-regulate the immune system. For it is only where the virus encounters an immunocompromised ‘host’ that it can run rampant!

Therefore, you should maintain the necessary respect for the virus and, in addition to the prescribed precautions, strengthen your immune system with a healthy lifestyle to give your body better protection against a serious infection. Make sure you try to reduce inflammation in your body with the help of healthy diet, adequate sleep, physical exercise and stress reduction. This can not only strengthen your immune system against viruses of all kinds, but also protect your brain from memory loss!

In this context, a conversation between Prof. Spitz and pharmacist Gröber is also worth seeing and hearing, in which the topic is: Corona, Influenza & Co – How do I strengthen my defenses!

 

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With this newsfeed the team of ‘Competence instead of dementia’ says goodbye to you for this year and would like to thank you for your trust and support in 2021!

We wish you a merry and blessed Christmas and

much happiness and above all continued good health in 2022!

🎄🎅🎄🤶🎄

 

References:

  1. Butowt R, Bilinska K. (2020) SARS-CoV-2: olfaction, brain infection, and the urgent need for clinical samples allowing earlier virus detection. ACS Chem Neurosci.11(9):1200-1203
  2. Liotta EM, Batra A, Clark JR, Shlobin NA, Hoffman SC, Orban ZS, Igor J Koralnik IJ (2020) Frequent neurologic manifestations and encephalopathy-associated morbidity in Covid-19 patients. Ann Clin Transl Neurol. Nov 7(11):2221-2230. doi: 10.1002/acn3.51210.
  3. Ragheb J, McKinney A, Zierau M, Brooks J, Hill-Caruthers M, Iskander M, Ahmed Y, Lobo R, Mentz L, Vlisides PE (2021) Delirium and neuropsychological outcomes in critically Ill patients with Covid-19: a cohort study BMJ Open Sep17;11(9):e050045. DOI: 10.1136/bmjopen-2021-050045
  4. Gabriel A. de Erausquin, Heather Snyder, María Carrillo, Akram A. Hosseini, Traolach S. Brugha, Sudha Seshadri, the CNS SARS-CoV-2 Consortium(2021) The chronic neuropsychiatric sequelae of Covid-19: The need for a prospective study of viral impact on brain functioning. Alzheimer’s Dement.17:1056–1065. DOI: 10.1002/alz.12255
  5. Yadi Zhou Y, Jielin Xu J, Hou Y, Leverenz JB, Kallianpur A, Mehra R, Liu R, Yu H, Pieper AA, Jehi L, Cheng F (2021) Network medicine links SARS-CoV-2/Covid-19 infection to brain microvascular injury and neuroinflammation in dementia-like cognitive impairment. Alzheimers Res Ther 9; 13(1): 110. DOI: 10.1186/s13195-021-00850-3
  6. Cantuti-Castelvetri, R Ojha, LD Pedro et al.
  7. Bhaskar S, Sinha A, Banach M, et al. (2020) Cytokine storm in Covid-19- immunopathological mechanisms, clinical considerations, and therapeutic approaches: the REPROGRAM consortium position paper. Front Immunol. 11:1648. https://doi.org/10.3389/fimmu.2020.01648

 

 

 

 

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