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REVIEW ARTICLE

SARS-CoV-2 and its long-term neurological impact: Unraveling the mechanisms of neurodegeneration and cognitive decline

Moawiah M. Naffaa1,2*
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1 Department of Cell Biology, Duke University School of Medicine, Durham, North Carolina, United States of America
2 Department of Psychology and Neuroscience, Trinity College of Arts and Sciences, Duke University, Durham, North Carolina, United States of America
Advanced Neurology, 4909 https://doi.org/10.36922/an.4909
Submitted: 23 September 2024 | Revised: 5 December 2024 | Accepted: 26 December 2024 | Published: 9 January 2025
© 2025 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
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Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19), is associated with neurological effects that persist beyond the acute phase, collectively referred to as post-acute sequelae of SARS-CoV-2 infection (PASC) or “long COVID.” This article discusses the neurological impacts of PASC, which can occur regardless of the initial illness’s severity. Studies indicate that most patients continue to experience symptoms for at least 3 months post-infection. Long-term effects include neurocognitive deficits, sleep disturbances, and the exacerbation of pre-existing conditions. Proposed mechanisms underlying these effects include neuroinflammation, microvascular damage, and autoimmune responses, while direct viral neuroinvasion remains a topic of ongoing debate. SARS-CoV-2 may also worsen pre-existing neurological disorders and increase the risk of developing neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease. The article highlights the need for longitudinal studies to better understand the variability in outcomes and the mechanisms driving these persistent effects. In addition, it explores the inflammatory pathways linking long COVID to AD. Both conditions are characterized by chronic inflammation, activation of shared markers such as the NLR family pyrin domain containing 3 inflammasome, and alterations in amyloid-beta production. The apolipoprotein E4 gene, a known risk factor for AD, is also associated with more severe COVID-19 outcomes. Neuroimaging studies reveal brain changes in COVID-19 survivors, particularly in regions related to cognition and memory, further emphasizing the need for long-term research to assess the potential role of long COVID in exacerbating neurodegenerative diseases.

Graphical abstract
Keywords
SARS-CoV-2
Long COVID
Neurodegenerative diseases
Cognitive decline
Inflammatory pathways
Autoimmune responses
Alzheimer’s disease
Neuro-post-acute sequelae of SARS-CoV-2 infection
Funding
None.
Conflict of interest
The author declares no conflicts of interest.
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Advanced Neurology, Electronic ISSN: 2810-9619 Print ISSN: 3060-8589, Published by AccScience Publishing
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