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Shared Mechanisms of Blood-Brain Barrier Dysfunction and Neuroinflammation in Coronavirus Disease 2019 and Alzheimer Disease
Meredith G. Mayer, Tracy Fischer. American Journal Of Pathology, 2025-04-18
Topic: Amyloid, tau and blood-test diagnosis
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), highlighted the virus's impact on the central nervous system and its potential to exacerbate neurodegenerative diseases, similar to that in Alzheimer disease (AD). Emerging evidence suggests that SARS-CoV-2 infection contributes to chronic neuroinflammation, a key driver in the etiopathogenesis of AD. Shared mechanisms, including blood-brain barrier (BBB) dysfunction, systemic inflammation, and activation of immune pathways, may link SARS-CoV-2 infection to AD onset and/or progression, particularly among vulnerable individuals, such as those of advanced age. This review explores convergent pathways involving the renin-angiotensin-aldosterone system, Wnt/β-catenin signaling, NF-κB activation, and interferon signaling, focusing on their roles in BBB integrity and neuroinflammation. SARS-CoV-2-mediated angiotensin-converting enzyme 2 depletion disrupts renin-angiotensin-aldosterone system homeostasis, favoring proinflammatory signaling that parallels vascular dysfunction in AD. Dysregulation of Wnt/β-catenin signaling exacerbates BBB permeability, whereas NF-κB and interferon pathways contribute to BBB breakdown and propagate central nervous system inflammation via endothelial and immune cell activation. These interactions may amplify prodromal AD pathology and/or initiate AD pathogenesis. By identifying mechanistic overlaps between COVID-19 and AD, this review underlines the need for therapeutic strategies targeting shared pathways of inflammation and BBB dysfunction. Understanding these connections is critical for mitigating the long-term neurologic sequelae of COVID-19 and reducing the burden of AD.
Key findings
- Emerging evidence suggests that SARS-CoV-2 infection contributes to chronic neuroinflammation, a key driver in the etiopathogenesis of AD.
Why it matters
This review explores shared mechanisms such as blood-brain barrier dysfunction and neuroinflammation that may link SARS-CoV-2 infection to Alzheimer's disease onset or progression. It proposes convergent pathways but does not show that COVID-19 causes Alzheimer's or that any treatment prevents it.
Study details
- Evidence strengthLow
How this study scored 42/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (American Journal Of Pathology) |
| Journal's citation record | 3 / 4 | American Journal Of Pathology: journal h-index 328 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2025 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 20 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.7 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 6.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 20 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Tracy Fischer: h-index 25 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Tulane University: institution h-index 735 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40254131) |
| Free to read | 2 / 2 | Free to read |
| Total | 42 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.ajpath.2025.03.011
- PubMed: 40254131
- Original source →
- Free full text: American Journal Of Pathology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Mayer, M. G., & Fischer, T. (2025). Shared Mechanisms of Blood-Brain Barrier Dysfunction and Neuroinflammation in Coronavirus Disease 2019 and Alzheimer Disease. American Journal Of Pathology. https://doi.org/10.1016/j.ajpath.2025.03.011
Vancouver
Mayer MG, Fischer T. Shared Mechanisms of Blood-Brain Barrier Dysfunction and Neuroinflammation in Coronavirus Disease 2019 and Alzheimer Disease. American Journal Of Pathology. 2025. doi:10.1016/j.ajpath.2025.03.011. PMID: 40254131.
BibTeX
@article{mayer2025-40254131,
author = {Mayer, Meredith G. and Fischer, Tracy},
title = {{Shared Mechanisms of Blood-Brain Barrier Dysfunction and Neuroinflammation in Coronavirus Disease 2019 and Alzheimer Disease}},
journal = {American Journal Of Pathology},
year = {2025},
doi = {10.1016/j.ajpath.2025.03.011},
pmid = {40254131},
url = {https://doi.org/10.1016/j.ajpath.2025.03.011}
}
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