Evidence map›Paper›PMID 42694660›Full record

ReviewFrontiers in aging neuroscience2026

Herpes simplex virus infection and Alzheimer's disease.

Ji-Yeun Hur

Abstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Ji-Yeun HurDepartment of Biological Sciences, Ajou University, Suwon, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over 95% of Alzheimer's disease (AD) is caused by a complex mixture of genetic and environmental factors. This is called sporadic AD or late-onset AD, and much of its pathological mechanisms remain unclear. There is growing evidence indicating that the viral infection, such as herpes simplex virus type 1 (HSV-1), triggers and worsens the AD progression in combination with the APOE4 genotype in AD patients. The innate immunity of host cells produces proinflammatory cytokines, which further drive neuroinflammation in the brain. Concurrently, Aβ and phosphorylated tau could entrap foreign pathogens such as HSV-1 according to the "antimicrobial protection hypothesis of AD," and accelerate the progression of AD. In this review, growing evidence ranging from HSV-1 infection to the AD progression via the accumulation of Aβ and tau, and neuroinflammation is explored.

Indexed as

Alzheimer’s diseaseamyloid betaantimicrobial peptideherpes simplex virusneuroinflammationneurotropic virustauviral infection

Identifiers

PMID42694660
PMCPMC13539487

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.