Current evidence that vitamin D is effective against COVID-19 neurological sequelae

recently life science In the study, researchers analyze the available scientific evidence to support vitamin D as a neuroprotective agent for the neurological sequelae of coronavirus disease 2019 (COVID-19).

study: COVID-19 and neurological sequelae: Vitamin D as a potential neuroprotective and / or neurorepairing agent.. Image Credits: Komarina / Shutterstock.com

Background

The infectivity of coronavirus 2 (SARS-CoV-2) for severe acute respiratory syndrome is not limited to the respiratory system. In fact, SARS-CoV-2 can also invade other important organs, including the central nervous system (CNS), which can have some neurological consequences.

Neurological symptoms of SARS-CoV-2 infection include immune demyelinating disease, anxiety, stroke, depression, and neurodegenerative disease. Two possible reasons for SARS-CoV-2 to attack CNS are its ability to remain latent in cells for extended periods of time. Cytokine storm..

These neurological conditions can be exacerbated in patients with COVID-19 with underlying chronic conditions such as hypertension, diabetes, or coronary heart disease. As a result, this subset of COVID-19 patients are more likely to experience neurovascular sequelae of the disease.

There is considerable scientific evidence that vitamin D downmodulates the effects of neuroinflammatory cytokines and diminishes the adverse effects of COVID-19. In particular, vitamin D also has other anti-inflammatory / immunomodulatory effects.

In a current meta-analysis covering 54 independent studies examining the literature on COVID-19 and vitamin D, researchers found that patients with low 25-hydroxyvitamin D levels were admitted to hospital associated with SARS-CoV-2 infection. We have found that it is more sensitive to it. These patients were also at increased risk of acute respiratory illness, hospitalization, and SARS-CoV-2 associated mortality.

Neuroinflammation and neurodegeneration in COVID-19

Due to the cytokine storm, some COVID-19 patients have reported acute necrotizing hemorrhagic encephalopathy. During SARS-CoV-2 infiltration of inflammatory cytokines including dendritic cells, monocytes, macrophages, and tumor necrosis factor-α (TNF-α), interleukin-1 and 6 (IL-1 and IL-6) Overexpressed in.

Because these biomarkers are associated with increased severity of COVID-19 and the resulting neurological pathology, monitoring these biomarkers can help classify the most severely ill patients and provide appropriate treatment options. Can be selected.

In one study of more than 30,000 healthy individuals, autoantibody titers against type 1 interferon (IFN) increased with age. This finding explains why older people tend to have a worse prognosis for COVID-19 and its neuropathological consequences.

Such incubation periods are associated with apoptosis of nervous system cells and delayed oxidative stress pathways, as brain cells may function as potential reservoirs for SARS-CoV-2, and nerves such as Alzheimer’s disease (AD). It can lead to degenerative conditions. Other reports suggest that SARS-CoV-2 increases α-synuclein synthesis and causes the release of various cytokines and chemokines that are characteristic of Parkinson’s disease (PD).

The SARS-CoV-2-induced neuroinflammatory response is associated with a marked decrease in human angiotensin converting enzyme 2 (hACE2) activity. hACE2 regulates host neuroprotection and neuroimmunomodulatory function and may neutralize cellular inflammation and oxidative stress.

In addition, SARS-CoV-2-ACE2 binding alters gamma-aminobutyric acid (GABA) neurotransmission in the amygdala and possibly other parts of the brain. Alternatively, it can cause changes in dopaminergic neurotransmission and represent other neurodegenerative sequelae associated with COVID-19.

Antibodies to the SARS-CoV-2 epitope have also been shown to react with receptors at the neuromuscular junction, including nicotinic acetylcholine. Therefore, this activity may accelerate COVID-19-related neurodegenerative conditions such as myasthenia gravis.

Vitamin D supplementation minimizes COVID-19-related neurological sequelae

Several studies have investigated vitamin D and 25-hydroxyvitamin D3 (calcifediol) as new treatment options for COVID-19-related neurological conditions. In fact, this type of supplement has been shown to enhance innate immunity, such as the initial macrophage response to mucosal invading viruses and bacteria, thereby reducing the incidence and severity of acute respiratory infections.

Sufficient plasma levels of 25-hydroxyvitamin D are converted to the hormone 1,25-dihydroxyvitamin D, activating genes encoding antibacterial substances against fungi, bacteria, and viruses, including SARS-CoV-2.

In their study, Durant et al. Vitamin D3 supplementation has been shown to efficiently induce gene expression associated with type I and type II IFN activity. This is important for the congenital response to bacterial and viral infections. Similarly, 1,25 (OH) 2D inhibits the action of renin by increasing hACE2 production, while reducing the cytokine storm-induced cell-mediated immune response during SARS-CoV-2-induced pneumonia. Let me.

Several clinical studies are also in the process of assessing possible optimizations for the SARS-CoV-2 vaccine. Effectiveness By vitamin D supplementation.

Conclusion

In summary, data from several studies support the use of vitamin D supplements and their role in improving the prognosis of the disease and preventing fatal consequences.

In the future, longitudinal studies will need to follow up with COVID-19 patients and collect the data needed to assess the diagnosis, prognosis, and treatment of COVID-19-related neurological sequelae. Meanwhile, the study also needs to monitor current COVID-19 patients and those who have recovered from the disease with vitamin D supplementation.

In conclusion, Vitamin D could be a valuable addition to current therapeutic weapons for COVID-19 neurological sequelae.