The molecular fingerprint of Neuroinflammation in COVID-19: A comprehensive discussion on molecular mechanisms of Neuroinflammation due to SARS-COV2 antigens.

The molecular fingerprint of Neuroinflammation in COVID-19: A comprehensive discussion on molecular mechanisms of Neuroinflammation due to SARS-COV2 antigens.

Publication date: Jan 19, 2024

Severe acute respiratory syndrome coronavirus 2 attacks the neural system directly and indirectly via various systems, such as the nasal cavity, olfactory system, and facial nerves. Considering the high energy requirement, lack of antioxidant defenses, and high amounts of metal ions in the brain, oxidative damage is very harmful to the brain. Various neuropathic pain conditions, neurological disorders, and neuropsychiatric complications were reported in Coronavirus disease 2019, prolonged Coronavirus disease 2019, and after Coronavirus disease 2019 immunization. This manuscript offers a distinctive outlook on the interconnectedness between neurology and neuropsychiatry through its meticulous analysis of complications. After recovering from Coronavirus disease 2019, approximately half of the patients reported developing Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Long Coronavirus disease 2019 imaging reports illustrated the hypometabolism in various parts of the brain, such as olfactory bulbs, limbic/paralimbic domains, the brainstem, and the cerebellum. Ninety imaging and neuropathological studies of Coronavirus disease 2019 have shown evidence of white matter, brainstem, frontotemporal, and oculofrontal lesions. Emotional functions, such as pleasant, long/short-term memory, movement, cognition and cognition in decision-making are controlled by these regions. The neuroinflammation and the mechanisms of defense are well presented in the discussion. The role of microglia activation, Inducible NO synthase, Cyclooxygenases 1/2 , Reactive oxygen species, neurotoxic toxins and pro-inflammatory cytokines, such as Interleukin-1 beta, Interleukin-6 and Tumor Necrosis Factor-alpha are highlighted in neuronal dysfunction and death. Nuclear factor kappa-light-chain-enhancer of activated B cells, Mitogen-activated protein kinase, Activator Protein 1, and Interferon regulatory factors are the main pathways involved in microglia activation in Coronavirus disease 2019 neuroinflammation. The neurological aspect of Coronavirus disease 2019 should be highlighted. Neurological, psychological, and behavioral aspects of Coronavirus disease 2019, prolonged Coronavirus disease 2019, and Coronavirus disease 2019 vaccines can be the upcoming issues. We need a global awareness where this aspect of the disease should be more considered in health research.

Concepts Keywords
Coronavirus Coronavirus disease 2019
Cyclooxygenases Molecular mechanism
Meticulous neuro-immune response
Necrosis

Semantics

Type Source Name
disease MESH Neuroinflammation
disease MESH COVID-19
disease VO Severe acute respiratory syndrome coronavirus 2
disease VO LACK
disease MESH oxidative damage
disease MESH neuropathic pain
disease MESH neurological disorders
disease MESH complications
disease VO immunization
disease MESH Myalgic Encephalomyelitis
disease MESH death
disease IDO immune response

Original Article

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