Coronavirus Disease 2019 (COVID-19) and Its Neuroinvasive Capacity: Is It Time for Melatonin?

Romero, Alejandro; Ramos, Eva; López-Muñoz, Francisco; Gil‐Martín, Emilio; Escames, Germaine; Reíter, Russel J.

doi:10.1007/s10571-020-00938-8

Cited by 29 publications

(20 citation statements)

References 132 publications

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“…In patients with severe COVID-19 disease, neurological complications comprising anosmia, stroke, paralysis, cranial nerve deficits, encephalopathy, delirium, meningitis, and seizures have been documented (see, for example, [ 64 , 96 ]). It remains to be established whether neurological abnormalities are caused by SARS-CoV-2 itself, by the exaggerated cytokine response it triggers, and/or by the increased formation of blood clots in brain blood vessels.…”

Section: Melatonin and Neuroprotectionmentioning

confidence: 99%

Can Melatonin Be a Potential “Silver Bullet” in Treating COVID-19 Patients?

2020

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The therapeutic potential of melatonin as a chronobiotic cytoprotective agent to counteract the consequences of COVID-19 infections has been advocated. Because of its wide-ranging effects as an antioxidant, anti-inflammatory, and immunomodulatory compound, melatonin could be unique in impairing the consequences of SARS-CoV-2 infection. Moreover, indirect evidence points out to a possible antiviral action of melatonin by interfering with SARS-CoV-2/angiotensin-converting enzyme 2 association. Melatonin is also an effective chronobiotic agent to reverse the circadian disruption of social isolation and to control delirium in severely affected patients. As a cytoprotector, melatonin serves to combat several comorbidities such as diabetes, metabolic syndrome, and ischemic and non-ischemic cardiovascular diseases, which aggravate COVID-19 disease. In view of evidence on the occurrence of neurological sequels in COVID-19-infected patients, another putative application of melatonin emerges based on its neuroprotective properties. Since melatonin is an effective means to control cognitive decay in minimal cognitive impairment, its therapeutic significance for the neurological sequels of SARS-CoV-2 infection should be considered. Finally, yet importantly, exogenous melatonin can be an adjuvant capable of augmenting the efficacy of anti-SARS-CoV-2 vaccines. We discuss in this review the experimental evidence suggesting that melatonin is a potential “silver bullet” in the COVID 19 pandemic.

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Section: Melatonin and Neuroprotectionmentioning

confidence: 99%

Can Melatonin Be a Potential “Silver Bullet” in Treating COVID-19 Patients?

2020

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“…Более того, Li Y-C. с соавт. [51] выдвинули гипотезу, что нейроинвазивный потенциал SARS-CoV-2 может, частично объяснить острую дыхательную недостаточность у пациентов с COVID-19 [74].…”

Section: неврологческие проявления Covid-19 как предпосылки для изучеunclassified

“…Таким образом, можно полагать, области мозга с наибольшей экспрессией рецепторов АПФ2 могут оказаться более подверженным инфицированию SARS-CoV-2, хотя участие других рецепторов или корецепторов однозначно не исключено [74].…”

Section: возможные пути и механизмы проникновения Sars-cov-2 в цнсunclassified

“…Возникает вопрос: может ли инфекция SARS-CoV-2 вызвать цитокиновый шторм в мозге? [74]. В свете недавних сообщений о случаях заболевания COVID-19, описывающих редкую форму тяжелого поражения мозга с гемофагоцитарным лимфогистиоцитозом [73] и пациенте с острой некротической геморрагической энцефалопатией [72], следует учитывать, что инфекция COVID-19 может вызвать «синдром цитокинового шторма» в головном мозге [58].…”

Section: молекулярные и клеточные мезанизмы альтерации и нейровоспаленияunclassified

“…Как показали недавние исследования, цитокиновый шторм вызывает повреждение ГЭБ при COVID-19, что приводит к усугублению течения нейровоспалительных заболеваний и нейротравм [76]. Целостность ГЭБ имеет решающее значение для поддержания функционирования ЦНС, и поэтому некоторые неврологические расстройства дебютируют после его повреждения [74].…”

Section: молекулярные и клеточные мезанизмы альтерации и нейровоспаленияunclassified

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Molecular and cellular mechanisms of central nervous system alteration in COVID-19

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Sokolov

Никитюк

et al. 2020

Žurnal anatomii i gistopatologii

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The ongoing coronavirus disease 2019 (COVID-19) pandemic dictates the need to study the molecular and cellular mechanisms of interaction between the pathogen and the human body. The manifestation of neurological symptoms in some patients with COVID-19 is a problem for neuroscientists due to the insufficiently understood pathomorphogenesis of the disease. This review systematizes the literature data reflecting the ways of penetration of SARS-CoV-2 into the brain, features of its interaction with neurons, neuroglia, and immune cells. It has been shown that the main mechanisms of SARS-CoV-2 neuroinvasion are presumably retrograde axonal transport along the fibers of the olfactory and vagus nerves; penetration through the damaged blood-brain barrier (BBB) or migration of immunocompetent cells containing viral particles through the intact BBB. It was found that virusinducible neuronal death is caused not only by a direct cytotoxic effect, but also due to dysregulation of the reninangiotensin system of the brain and the release of a large amount of inflammatory cytokines as a manifestation of a “cytokine storm”. The participation of neuroglial cells in the initiation and maintenance of neuroinflammatory and neurodegenerative processes due to the activation of their proinflammatory phenotype has been demonstrated. The role of mast cells in antiviral defense mechanisms and inflammatory reactions is discussed.

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