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Review
. 2022 Sep 22;11(19):2959.
doi: 10.3390/cells11192959.

Neuroinflammation in Dementia-Therapeutic Directions in a COVID-19 Pandemic Setting

Mateusz Łuc  1 , Marta Woźniak  2 , Joanna Rymaszewska  1
Affiliations
Review

Neuroinflammation in Dementia-Therapeutic Directions in a COVID-19 Pandemic Setting

Mateusz Łuc et al. Cells. .

Abstract

Although dementia is a heterogenous group of diseases, inflammation has been shown to play a central role in all of them and provides a common link in their pathology. This review aims to highlight the importance of immune response in the most common types of dementia. We describe molecular aspects of pro-inflammatory signaling and sources of inflammatory activation in the human organism, including a novel infectious agent, SARS-CoV-2. The role of glial cells in neuroinflammation, as well as potential therapeutic approaches, are then discussed. Peripheral immune response and increased cytokine production, including an early surge in TNF and IL-1β concentrations activate glia, leading to aggravation of neuroinflammation and dysfunction of neurons during COVID-19. Lifestyle factors, such as diet, have a large impact on future cognitive outcomes and should be included as a crucial intervention in dementia prevention. While the use of NSAIDs is not recommended due to inconclusive results on their efficacy and risk of side effects, the studies focused on the use of TNF antagonists as the more specific target in neuroinflammation are still very limited. It is still unknown, to what degree neuroinflammation resulting from COVID-19 may affect neurodegenerative process and cognitive functioning in the long term with ongoing reports of chronic post-COVID complications.

Keywords: COVID-19; SARS-CoV-2; TNF; TNF antagonists; glial cells; neuroinflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
SARS-CoV-2 infection impacts the CNS via several potential pathways: (1) Infection of endothelial cells by viral particles present in the blood; (2) infiltration of the CNS by activated leukocytes from the bloodstream; (3) entrance of pro-inflammatory cytokines into the CNS; (4) loss of the BBB integrity due to increased immune response; (5) hypothetic direct passage of viral particles via olfactory nerve and (6) activation of pro-inflammatory phenotypes of CNS-residing cells.
See this image and copyright information in PMC

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