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Review
. 2022 Feb;272(1):139-154.
doi: 10.1007/s00406-021-01286-4. Epub 2021 Jun 25.

Cognitive decline following acute viral infections: literature review and projections for post-COVID-19

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Review

Cognitive decline following acute viral infections: literature review and projections for post-COVID-19

Rodolfo Furlan Damiano et al. Eur Arch Psychiatry Clin Neurosci. 2022 Feb.

Abstract

Recently, much attention has been drawn to the importance of the impact of infectious disease on human cognition. Several theories have been proposed, to explain the cognitive decline following an infection as well as to understand better the pathogenesis of human dementia, especially Alzheimer's disease. This article aims to review the state of the art regarding the knowledge about the impact of acute viral infections on human cognition, laying a foundation to explore the possible cognitive decline followed coronavirus disease 2019 (COVID-19). To reach this goal, we conducted a narrative review systematizing six acute viral infections as well as the current knowledge about COVID-19 and its impact on human cognition. Recent findings suggest probable short- and long-term COVID-19 impacts in cognition, even in asymptomatic individuals, which could be accounted for by direct and indirect pathways to brain dysfunction. Understanding this scenario might help clinicians and health leaders to deal better with a wave of neuropsychiatric issues that may arise following COVID-19 pandemic as well as with other acute viral infections, to alleviate the cognitive sequelae of these infections around the world.

Keywords: Alzheimer’s disease; COVID-19; Cognition; Dementia; Prevention; Virus.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1
Fig. 1
Proposed pathophysiological mechanisms of the impact of SARS-CoV-2 infection on human cognition. First, risk factors, such as genetic, lifestyle, inflammatory diseases and previous viral and bacterial infections, might interact with exposure to SARS-CoV-2 in brains of both cognitively healthy and impaired individuals. It may induce several different mechanisms, such as neuro-inflammation, cytokine cascade, hypercoagulability, direct brain injury, astrocytes infection, epigenetic changes and oxidative stress, which together may induce medical-temporal lobe abnormalities and/or increased amyloid-β. These different pathways might induce a cognitive impairment, mainly in executive, attentional, language and working memory areas

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