SARS-CoV-2 (COVID-19) as a Predictor of Neuroinflammation and Neurodegeneration: Potential Treatment Strategies

Путилина, М. В.; Grishin, D. V.

doi:10.1007/s11055-021-01108-z

Cited by 8 publications

(4 citation statements)

References 44 publications

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“…The latter is characterized by high serum levels of pro-inflammatory biomarkers (such as CRP, IL-6, etc.) and by an uncontrolled inflammatory process that, if not inhibited, induces multi-organ failure [46][47][48]. Therefore, the significant reduction in inflammatory status that we observed in our um-PEA-treated patients seems to contrast the onset of the systemic inflammation and the CS.…”

Section: Discussionmentioning

confidence: 63%

Effects of Ultramicronized Palmitoylethanolamide (um-PEA) in COVID-19 Early Stages: A Case–Control Study

et al. 2022

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Ultramicronized palmitoylethanolamide (um-PEA), a compound with antioxidant, anti-inflammatory and neuroprotective properties, appears to be a potential adjuvant treatment for early stages of Coronavirus disease 2019 (COVID-19). In our study, we enrolled 90 patients with confirmed diagnosis of COVID-19 that were randomized into two groups, homogeneous for age, gender and BMI. The first group received oral supplementation based on um-PEA at a dose of 1800 mg/day for a total of 28 days; the second group was the control group (R.S. 73.20). At baseline (T0) and after 28 days of um-PEA treatment (T1), we monitored: routine laboratory parameters, inflammatory and oxidative stress (OS) biomarkers, lymphocytes subpopulation and COVID-19 serological response. At T1, the um-PEA-treated group presented a significant reduction in inflammation compared to the control group (CRP p = 0.007; IL-6 p = 0.0001; neutrophils to lymphocytes ratio p = 0.044). At T1, the controls showed a significant increase in OS compared to the treated group (FORT p = 0.05). At T1, the um-PEA group exhibited a significant decrease in D-dimer levels (p = 0.0001) and higher levels of IgG against SARS-CoV-2 (p = 0.0001) compared to the controls. Our data demonstrated, in a randomized clinical trial, the beneficial effects of um-PEA in both asymptomatic and mild-symptomatic patients related to reductions in inflammatory state, OS and coagulative cascade alterations.

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Section: Discussionmentioning

confidence: 63%

Effects of Ultramicronized Palmitoylethanolamide (um-PEA) in COVID-19 Early Stages: A Case–Control Study

et al. 2022

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“…So far, anti-inflammatory therapy has not been shown to be useful in affecting long COVID cognitive function, including dexamethasone, and tocilizumab ( 70 , 71 ).…”

Section: Evaluation Of the Hypothesismentioning

confidence: 99%

Refueling the post COVID-19 brain: potential role of ketogenic medium chain triglyceride supplementation: an hypothesis

2023

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COVID-19 infection causes cognitive changes in the acute phase, but also after apparent recovery. Over fifty post (long)-COVID symptoms are described, including cognitive dysfunction (“brain fog”) precluding return to pre-COVID level of function, with rates twice as high in females. Additionally, the predominant demographic affected by these symptoms is younger and still in the workforce. Lack of ability to work, even for six months, has significant socio-economic consequences. This cognitive dysfunction is associated with impaired cerebral glucose metabolism, assessed using 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET), showing brain regions that are abnormal compared to age and sex matched controls. In other cognitive conditions such as Alzheimer’s disease (AD), typical patterns of cerebral glucose hypometabolism, frontal hypometabolism and cerebellar hypermetabolism are common. Similar FDG-PET changes have also been observed in post-COVID-19, raising the possibility of a similar etiology. Ketone bodies (B-hydroxybutyrate, acetoacetate and acetone) are produced endogenously with very low carbohydrate intake or fasting. They improve brain energy metabolism in the face of cerebral glucose hypometabolism in other conditions [mild cognitive impairment (MCI) and AD]. Long-term low carbohydrate intake or prolonged fasting is not usually feasible. Medium chain triglyceride (MCT) is an exogenous route to nutritional ketosis. Research has supported their efficacy in managing intractable seizures, and cognitive impairment in MCI and AD. We hypothesize that cerebral glucose hypometabolism associated with post COVID-19 infection can be mitigated with MCT supplementation, with the prediction that cognitive function would also improve. Although there is some suggestion that post COVID-19 cognitive symptoms may diminish over time, in many individuals this may take more than six months. If MCT supplementation is able to speed the cognitive recovery, this will impact importantly on quality of life. MCT is readily available and, compared to pharmaceutical interventions, is cost-effective. Research shows general tolerability with dose titration. MCT is a component of enteral and parenteral nutrition supplements, including in pediatrics, so has a long record of safety in vulnerable populations. It is not associated with weight gain or adverse changes in lipid profiles. This hypothesis serves to encourage the development of clinical trials evaluating the impact of MCT supplementation on the duration and severity of post COVID-19 cognitive symptoms.

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“…In a study conducted in vitro, it was found that infection with SARS-CoV-2 led to an increase in the levels of CX3CL1, also known as fractalkine (FKN) (Blanco-Melo et al, 2020). The release of chemokines in response to neuroinflammation can set off a cascade of signaling pathways, one of which is oxidative stress, which ultimately results in the death of neurons (Putilina & Grishin, 2021).…”

Section: Effec Ts Of Covid -19-induced Immune Re S P On S E On the B B Bmentioning

confidence: 99%

A review of the mechanisms of blood–brain barrier disruption during COVID‐19 infection

Al-Obaidi

Desa

2023

J of Neuroscience Research

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Coronaviruses are prevalent in mammals and birds, including humans and bats, and they often spread through airborne droplets. In humans, these droplets then interact with angiotensin‐converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), which are the main receptors for the SARS‐CoV‐2 virus. It can infect several organs, including the brain. The blood–brain barrier (BBB) is designed to maintain the homeostatic neural microenvironment of the brain, which is necessary for healthy neuronal activity, function, and stability. It prevents viruses from entering the brain parenchyma and does not easily allow chemicals to pass into the brain while assisting numerous compounds in exiting the brain. The purpose of this review was to examine how COVID‐19 influences the BBB along with the mechanisms that indicate the BBB's deterioration. In addition, the cellular mechanism through which SARS‐CoV‐2 causes BBB destruction by binding to ACE2 was evaluated and addressed. The mechanisms of the immunological reaction that occurs during COVID‐19 infection that may contribute to the breakdown of the BBB were also reviewed. It was discovered that the integrity of the tight junction (TJs), basement membrane, and adhesion molecules was damaged during COVID‐19 infection, which led to the breakdown of the BBB. Therefore, understanding how the BBB is disrupted by COVID‐19 infection will provide an indication of how the SARS‐CoV‐2 virus is able to reach the central nervous system (CNS). The findings of this research may help in the identification of treatment options for COVID‐19 that can control and manage the infection.

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SARS-CoV-2 (COVID-19) as a Predictor of Neuroinflammation and Neurodegeneration: Potential Treatment Strategies

Cited by 8 publications

References 44 publications

Effects of Ultramicronized Palmitoylethanolamide (um-PEA) in COVID-19 Early Stages: A Case–Control Study

Effects of Ultramicronized Palmitoylethanolamide (um-PEA) in COVID-19 Early Stages: A Case–Control Study

Refueling the post COVID-19 brain: potential role of ketogenic medium chain triglyceride supplementation: an hypothesis

A review of the mechanisms of blood–brain barrier disruption during COVID‐19 infection

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