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HSV-1 as a Potential Driver of Alzheimer’s Disease
D Li, Eun Seok Choi, Xiaoyong Bao. Pathogens, 2025-10-08
Topic: Amyloid, tau and blood-test diagnosis
Herpes simplex virus type 1 (HSV-1) is a continuous health challenge, and current antiviral treatments cannot cure the virus. As life expectancy continues to increase worldwide, HSV-1 should remain a focus to minimize its associated health complications within the aging population. While often asymptomatic, HSV-1 causes oral and cutaneous lesions and establishes latency with periodic reactivation. Antivirals reduce symptoms but do not eradicate the virus. Emerging evidence links HSV-1 to Alzheimer's disease (AD) via chronic neuroinflammation, amyloid-beta and tau accumulation, oxidative stress, and synaptic dysfunction, with viral proteins detected in AD-affected brain regions. This review assesses the current evidence for HSV-1 in dementia pathogenesis, examines antiviral strategies as potential neuroprotective interventions, and outlines the experimental models required to establish causality.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Li, D., Choi, E. S., & Bao, X. (2025). HSV-1 as a Potential Driver of Alzheimer’s Disease. Pathogens. https://doi.org/10.3390/pathogens14101022
Vancouver
Li D, Choi ES, Bao X. HSV-1 as a Potential Driver of Alzheimer’s Disease. Pathogens. 2025. doi:10.3390/pathogens14101022. PMID: 41156633.
BibTeX
@article{li2025-41156633,
author = {Li, D and Choi, Eun Seok and Bao, Xiaoyong},
title = {{HSV-1 as a Potential Driver of Alzheimer’s Disease}},
journal = {Pathogens},
year = {2025},
doi = {10.3390/pathogens14101022},
pmid = {41156633},
url = {https://doi.org/10.3390/pathogens14101022}
}
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.
Key findings
- As life expectancy continues to increase worldwide, HSV-1 should remain a focus to minimize its associated health complications within the aging population.
- While often asymptomatic, HSV-1 causes oral and cutaneous lesions and establishes latency with periodic reactivation.
- Antivirals reduce symptoms but do not eradicate the virus.
- Emerging evidence links HSV-1 to Alzheimer's disease (AD) via chronic neuroinflammation, amyloid-beta and tau accumulation, oxidative stress, and synaptic dysfunction, with viral proteins detected in AD-affected brain regions.
- This review assesses the current evidence for HSV-1 in dementia pathogenesis, examines antiviral strategies as potential neuroprotective interventions, and outlines the experimental models required to establish causality.
Why it matters
This review assesses evidence linking HSV-1 to Alzheimer's disease through chronic neuroinflammation, amyloid-beta and tau accumulation, oxidative stress and synaptic dysfunction, and notes that antivirals reduce symptoms but do not eradicate the virus. It outlines experimental models needed to establish causality, so no antiviral is yet shown to prevent or treat Alzheimer's.
Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Pathogens) |
| Journal's citation record | 1 / 4 | Pathogens: journal h-index 120 (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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 2 / 7 | Cited 6 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 2.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 3.3× 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 | 1 / 4 | Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Xiaoyong Bao: h-index 32 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | The University of Texas Medical Branch at Galveston: institution h-index 655 (OpenAlex) |
| Multicenter 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 41156633) |
| Free to read | 2 / 2 | Free to read |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
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