COVID-19 as a Risk Factor for Alzheimer’s Disease
Open accessAbstract
Severe acute respiratory disease coronavirus 2 (SARS-CoV-2) is responsible for the coronavirus disease 2019 (COVID-19) pandemic. Although a primarily respiratory disease, recent reports indicate that it also affects the central nervous system (CNS). Over 25% of COVID-19 patients report neurological symptoms such as memory loss, anosmia, hyposmia, confusion, and headaches. The neurological outcomes may be a result of viral entry into the CNS and/or resulting neuroinflammation, both of which underlie an elevated risk for Alzheimer’s disease (AD). Herein, we ask: Is COVID-19 a risk factor for AD? To answer, we identify the literature and review mechanisms by which COVID-19-mediated neuroinflammation can contribute to the development of AD, evaluate the effects of acute versus chronic phases of infection, and lastly, discuss potential therapeutics to address the rising rates of COVID-19 neurological sequelae.
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COVID-19 patients with long or post-acute sequelae have increased risk of AD.
“Many COVID-19 patients diagnosed with some long or post-acute sequelae of COVID-19 such as brain atrophy and memory decline, greatly increasing the risk of AD.602,603”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [602]
In “Acute Versus Long COVID-19” (page unavailable), the paper reports persistent memory problems and proposes that post-acute sequelae may increase AD risk. It also reports brain-size reductions after infection in “Biomarkers of AD Neurodegeneration in Severe COVID-19.” But the Conclusion says no study has conclusively established whether long COVID-19 contributes to AD, so the citing sentence’s definite claim of a greatly increased risk overstates the evidence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSARS-CoV-2 entry may cause cytokine storms, immune dysregulation, BBB disruption, reduced Aβ clearance, leading to neuroinflammation and Aβ aggregation.
“Upon entry into the host cell, it may cause cytokine storms and immune dysregulation, disrupt the BBB, and reduce Aβ clearance, ultimately resulting in neuroinflammation and Aβ aggregation.602”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [602]
PLCG2 polymorphisms are associated with both reduced and increased risk of Alzheimer's disease and with longevity.
“PLCG2 polymorphisms are associated with both reduced and increased risk of Alzheimer’s disease (AD) and with longevity.”
From Multi-omics analyses reveal novel effects of PLCγ2 deficiency in the mouse brain (2023) · cites this paper as [5]
The ACE2 and APOE4 sections discuss genetic variants and Alzheimer’s disease risk, but neither addresses PLCG2 or longevity. Searches for PLCG2 polymorphisms and phospholipase C gamma 2 variants found no passage in our copy supporting the attributed associations; no page numbers were provided. (LLM, conf=0.76)
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- Authors
- Golzari-Sorkheh, M., Weaver, D. F., & Reed, M. A.
- Affiliations
- University of Toronto (CA)
- University Health Network (CA)
- Corresponding author
- Reed, Mark A.
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2023-01-03
- Volume
- 91
- Issue
- 1
- Pages
- 1-23
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W4307771970
- Cited by
- 39
- References
- 254
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 15 · 2023: 10
- FWCI
- 1.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Krembil Foundation
- Topics
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- COVID-19 pandemic, SARS-CoV-2
- MeSH terms
- COVID-19, SARS-CoV-2, Neuroinflammatory Diseases, Alzheimer Disease, Humans, Nervous System Diseases, Risk Factors
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